Pub Date : 2024-01-01Epub Date: 2023-06-24DOI: 10.1080/08830185.2023.2222769
Alisha Arora, Archana Singh
With the change in global environment, respiratory disorders are becoming more threatening to the health of people all over the world. These diseases are closely linked to performance of immune system. Within the innate arm of immune system, Neutrophils are an important moiety to serve as an immune defense barrier. They are one of the first cells recruited to the site of infection and plays a critical role in pathogenesis of various pulmonary diseases. It is established that the migration and activation of neutrophils can lead to inflammation either directly or indirectly and this inflammation caused is very crucial for the clearance of pathogens and resolution of infection. However, the immunopathological mechanisms involved to carry out the same is very complex and not well understood. Despite there being studies concentrating on the role of neutrophils in multiple respiratory diseases, there is still a long way to go in order to completely understand the complexity of the participation of neutrophils and mechanisms involved in the development of these respiratory diseases. In the present article, we have reviewed the literature to comprehensively provide an insight in the current development and advancements about the role of neutrophils in infectious respiratory disorders including viral respiratory disorders such as Coronavirus disease (COVID-19) and bacterial pulmonary disorders with a focused review on pulmonary tuberculosis as well as in noninfectious disorders like Chronic obstructive pulmonary disease (COPD) and asthma. Also, future directions into research and therapeutic targets have been discussed for further exploration.
{"title":"Exploring the role of neutrophils in infectious and noninfectious pulmonary disorders.","authors":"Alisha Arora, Archana Singh","doi":"10.1080/08830185.2023.2222769","DOIUrl":"10.1080/08830185.2023.2222769","url":null,"abstract":"<p><p>With the change in global environment, respiratory disorders are becoming more threatening to the health of people all over the world. These diseases are closely linked to performance of immune system. Within the innate arm of immune system, Neutrophils are an important moiety to serve as an immune defense barrier. They are one of the first cells recruited to the site of infection and plays a critical role in pathogenesis of various pulmonary diseases. It is established that the migration and activation of neutrophils can lead to inflammation either directly or indirectly and this inflammation caused is very crucial for the clearance of pathogens and resolution of infection. However, the immunopathological mechanisms involved to carry out the same is very complex and not well understood. Despite there being studies concentrating on the role of neutrophils in multiple respiratory diseases, there is still a long way to go in order to completely understand the complexity of the participation of neutrophils and mechanisms involved in the development of these respiratory diseases. In the present article, we have reviewed the literature to comprehensively provide an insight in the current development and advancements about the role of neutrophils in infectious respiratory disorders including viral respiratory disorders such as Coronavirus disease (COVID-19) and bacterial pulmonary disorders with a focused review on pulmonary tuberculosis as well as in noninfectious disorders like Chronic obstructive pulmonary disease (COPD) and asthma. Also, future directions into research and therapeutic targets have been discussed for further exploration.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":" ","pages":"41-61"},"PeriodicalIF":5.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10053452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1080/08830185.2021.1958806
Mohammad Reza Haghshenas, Hamid Ghaderi, Hossein Daneste, Abbas Ghaderi
Salivary glands naturally play central roles in oral immunity. The salivary glands microenvironment inevitable may be exposed to exogenous factors consequently triggering the initiation and formation of various malignant and benign tumors. Mesenchymal stem cells are recruited into salivary gland microenvironment, interact with tumor cells, and induce inhibitory cytokines as well as cells with immunosuppressive phenotypes such as myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs). The immune components and tumor immune responses in malignant and benign SGTs are still under investigation. Immune responses may directly play a limiting role in tumor growth and expansion, or may participate in formation of a rich milieu for tumor growth in cooperation with other cellular and regulatory molecules. Immune checkpoint molecules (e.g. PDLs, HLA-G and LAG3) are frequently expressed on tumor cells and/or tumor-infiltrating lymphocytes (TILs) in salivary gland microenvironment, and an increase in their expression is associated with T cell exhaustion, immune tolerance and tumor immune escape. Chemokines and chemokine receptors have influential roles on aggressive behaviors of SGTs, and thereby they could be candidate targets for cancer immunotherapy. To present a broad knowledge on salivary glands, this review first provides a brief description on immunological functions of normal salivary glands, and then describe the SGT's tumor microenvironment, by focusing on mesenchymal stem cells, immune cell subsets, immune checkpoint molecules, chemokines and chemokine receptors, and finally introduces immune checkpoint inhibitors as well as potential targets for cancer therapy.
{"title":"Immunological and biological dissection of normal and tumoral salivary glands.","authors":"Mohammad Reza Haghshenas, Hamid Ghaderi, Hossein Daneste, Abbas Ghaderi","doi":"10.1080/08830185.2021.1958806","DOIUrl":"https://doi.org/10.1080/08830185.2021.1958806","url":null,"abstract":"<p><p>Salivary glands naturally play central roles in oral immunity. The salivary glands microenvironment inevitable may be exposed to exogenous factors consequently triggering the initiation and formation of various malignant and benign tumors. Mesenchymal stem cells are recruited into salivary gland microenvironment, interact with tumor cells, and induce inhibitory cytokines as well as cells with immunosuppressive phenotypes such as myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs). The immune components and tumor immune responses in malignant and benign SGTs are still under investigation. Immune responses may directly play a limiting role in tumor growth and expansion, or may participate in formation of a rich milieu for tumor growth in cooperation with other cellular and regulatory molecules. Immune checkpoint molecules (e.g. PDLs, HLA-G and LAG3) are frequently expressed on tumor cells and/or tumor-infiltrating lymphocytes (TILs) in salivary gland microenvironment, and an increase in their expression is associated with T cell exhaustion, immune tolerance and tumor immune escape. Chemokines and chemokine receptors have influential roles on aggressive behaviors of SGTs, and thereby they could be candidate targets for cancer immunotherapy. To present a broad knowledge on salivary glands, this review first provides a brief description on immunological functions of normal salivary glands, and then describe the SGT's tumor microenvironment, by focusing on mesenchymal stem cells, immune cell subsets, immune checkpoint molecules, chemokines and chemokine receptors, and finally introduces immune checkpoint inhibitors as well as potential targets for cancer therapy.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"42 2","pages":"139-155"},"PeriodicalIF":5.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9455710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01Epub Date: 2022-05-18DOI: 10.1080/08830185.2022.2076846
Xiaoxiao Wu, Bing Gu, Huan Yang
The intestinal mucosa is an important structure involved in resistance to pathogen infection. It is mainly composed of four barriers, which have different but interrelated functions. Pathogenic bacteria can damage these intestinal mucosal barriers. Here, we mainly review the mechanisms of pathogen damage to biological barriers. Most γδ T cells are located on the surface of the intestinal mucosa, with the ability to migrate and engage in crosstalk with microorganisms. Commensal bacteria are involved in the activation and migration of γδ T cells to monitor the invasion of pathogens. Pathogen invasion alters the migration pattern of γδ T cells. γδ T cells accelerate pathogen clearance and limit opportunistic invasion of commensal bacteria. By discussing these interactions among γδ T cells, commensal bacteria and pathogenic bacteria, we suggest that γδ T cells may link the interactions between commensal bacteria and pathogenic bacteria.
{"title":"The role of γδ T cells in the interaction between commensal and pathogenic bacteria in the intestinal mucosa.","authors":"Xiaoxiao Wu, Bing Gu, Huan Yang","doi":"10.1080/08830185.2022.2076846","DOIUrl":"10.1080/08830185.2022.2076846","url":null,"abstract":"<p><p>The intestinal mucosa is an important structure involved in resistance to pathogen infection. It is mainly composed of four barriers, which have different but interrelated functions. Pathogenic bacteria can damage these intestinal mucosal barriers. Here, we mainly review the mechanisms of pathogen damage to biological barriers. Most γδ T cells are located on the surface of the intestinal mucosa, with the ability to migrate and engage in crosstalk with microorganisms. Commensal bacteria are involved in the activation and migration of γδ T cells to monitor the invasion of pathogens. Pathogen invasion alters the migration pattern of γδ T cells. γδ T cells accelerate pathogen clearance and limit opportunistic invasion of commensal bacteria. By discussing these interactions among γδ T cells, commensal bacteria and pathogenic bacteria, we suggest that γδ T cells may link the interactions between commensal bacteria and pathogenic bacteria.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"1 1","pages":"379-392"},"PeriodicalIF":5.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45397260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1080/08830185.2022.2064461
Surendra Gulla, Madhava C Reddy, Vajra C Reddy, Sriram Chitta, Manjula Bhanoori, Dakshayani Lomada
The thymus is a primary lymphoid organ, essential for the development of T-cells that will protect from invading pathogens, immune disorders, and cancer. The thymus decreases in size and cellularity with age referred to as thymus involution or atrophy. This involution causes decreased T-cell development and decreased naive T-cell emigration to the periphery, increased proportion of memory T cells, and a restricted, altered T-cell receptor (TCR) repertoire. The changes in composition and function of the circulating T cell pool as a result of thymic involution led to increased susceptibility to infectious diseases including the recent COVID and a higher risk for autoimmune disorders and cancers. Thymic involution consisting of both structural and functional loss of the thymus has a deleterious effect on T cell development, T cell selection, and tolerance. The mechanisms which act on the structural (cortex and medulla) matrix of the thymus, the gradual accumulation of genetic mutations, and altered gene expressions may lead to immunosenescence as a result of thymus involution. Understanding the molecular mechanisms behind thymic involution is critical for identifying diagnostic biomarkers and targets for treatment help to develop strategies to mitigate thymic involution-associated complications. This review is focused on the consequences of thymic involution in infections, immune disorders, and diseases, identifying potential checkpoints and potential approaches to sustain or restore the function of the thymus particularly in elderly and immune-compromised individuals.
{"title":"Role of thymus in health and disease.","authors":"Surendra Gulla, Madhava C Reddy, Vajra C Reddy, Sriram Chitta, Manjula Bhanoori, Dakshayani Lomada","doi":"10.1080/08830185.2022.2064461","DOIUrl":"https://doi.org/10.1080/08830185.2022.2064461","url":null,"abstract":"<p><p>The thymus is a primary lymphoid organ, essential for the development of T-cells that will protect from invading pathogens, immune disorders, and cancer. The thymus decreases in size and cellularity with age referred to as thymus involution or atrophy. This involution causes decreased T-cell development and decreased naive T-cell emigration to the periphery, increased proportion of memory T cells, and a restricted, altered T-cell receptor (TCR) repertoire. The changes in composition and function of the circulating T cell pool as a result of thymic involution led to increased susceptibility to infectious diseases including the recent COVID and a higher risk for autoimmune disorders and cancers. Thymic involution consisting of both structural and functional loss of the thymus has a deleterious effect on T cell development, T cell selection, and tolerance. The mechanisms which act on the structural (cortex and medulla) matrix of the thymus, the gradual accumulation of genetic mutations, and altered gene expressions may lead to immunosenescence as a result of thymus involution. Understanding the molecular mechanisms behind thymic involution is critical for identifying diagnostic biomarkers and targets for treatment help to develop strategies to mitigate thymic involution-associated complications. This review is focused on the consequences of thymic involution in infections, immune disorders, and diseases, identifying potential checkpoints and potential approaches to sustain or restore the function of the thymus particularly in elderly and immune-compromised individuals.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"42 5","pages":"347-363"},"PeriodicalIF":5.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10212393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1080/08830185.2016.1206098
Uzma Malik, Aneela Javed
Mammalian immune system is a complex amalgam of diverse cellular and noncellular components such as cytokines, receptors and co-receptors. FAM26F (family with sequence similarity 26, member F) is a recently identified tetraspanin-like membrane glycoprotein which is predicted to make homophilic interactions and potential synapses between several immune cells including CD4+, CD8+, NK, dendritic cells and macrophages. Various whole transcriptome analyses have demonstrated the differential expression of FAM26F in several bacterial, viral and parasitic infections, in certain pathophysiological conditions such as liver and heart transplantation, and in various cancers. The complete understanding of transcriptional regulation of FAM26F is in its infancy however it is up regulated by various stimulants such as polyI:C, LPS, INF gamma and TNF alpha, and via various proposed pathways including TLR3, TLR4 IFN-β and Dectin-1. These pathways can merge in STAT1 activation. The synergistic expression of FAM26F on both NK-cells and myeloid dendritic cells is required to activate NK-cells against tumors via its cytoplasmic tail, thus emphasizing therapeutic potential of FAM26F for NK sensitive tumors. Current review provides a comprehensive basis to propose that FAM26F expression level is at least a hallmark for IFN-γ-lead immune responses and thus can proficiently be regarded as an early diagnostic marker. Future investigation dissecting the role of FAM26F in activation of various immune cell populations in local amplification by cell-cell contact is crucial to provide the missing link imperative for elucidating the relevance of this protein in immune responses.
哺乳动物的免疫系统是一个由细胞因子、受体和共受体等多种细胞和非细胞成分组成的复杂混合体。FAM26F (family with sequence similarity 26, member F)是最近发现的一种类似四联蛋白(tetraspanin-like)的膜糖蛋白,可在多种免疫细胞(包括CD4+、CD8+、NK、树突状细胞和巨噬细胞)之间产生亲同质相互作用和潜在突触。各种全转录组分析已经证明FAM26F在几种细菌、病毒和寄生虫感染、某些病理生理条件(如肝脏和心脏移植)以及各种癌症中的差异表达。对FAM26F转录调控的全面了解尚处于起步阶段,但它受到多种刺激物的上调,如polyI:C、LPS、INF γ和TNF α,并通过各种被提出的途径,包括TLR3、TLR4、IFN-β和Dectin-1。这些通路可以在STAT1激活中合并。FAM26F在NK细胞和髓系树突状细胞上的协同表达是激活NK细胞抗肿瘤的必要条件,从而强调了FAM26F对NK敏感肿瘤的治疗潜力。目前的综述提供了全面的基础,提出FAM26F表达水平至少是IFN-γ-铅免疫反应的标志,因此可以熟练地视为早期诊断标志物。未来的研究剖析FAM26F在细胞与细胞接触的局部扩增中激活各种免疫细胞群中的作用,对于阐明该蛋白在免疫应答中的相关性至关重要。
{"title":"FAM26F: An Enigmatic Protein Having a Complex Role in the Immune System.","authors":"Uzma Malik, Aneela Javed","doi":"10.1080/08830185.2016.1206098","DOIUrl":"https://doi.org/10.1080/08830185.2016.1206098","url":null,"abstract":"<p><p>Mammalian immune system is a complex amalgam of diverse cellular and noncellular components such as cytokines, receptors and co-receptors. FAM26F (family with sequence similarity 26, member F) is a recently identified tetraspanin-like membrane glycoprotein which is predicted to make homophilic interactions and potential synapses between several immune cells including CD4<sup>+</sup>, CD8<sup>+</sup>, NK, dendritic cells and macrophages. Various whole transcriptome analyses have demonstrated the differential expression of FAM26F in several bacterial, viral and parasitic infections, in certain pathophysiological conditions such as liver and heart transplantation, and in various cancers. The complete understanding of transcriptional regulation of FAM26F is in its infancy however it is up regulated by various stimulants such as polyI:C, LPS, INF gamma and TNF alpha, and via various proposed pathways including TLR3, TLR4 IFN-β and Dectin-1. These pathways can merge in STAT1 activation. The synergistic expression of FAM26F on both NK-cells and myeloid dendritic cells is required to activate NK-cells against tumors via its cytoplasmic tail, thus emphasizing therapeutic potential of FAM26F for NK sensitive tumors. Current review provides a comprehensive basis to propose that FAM26F expression level is at least a hallmark for IFN-γ-lead immune responses and thus can proficiently be regarded as an early diagnostic marker. Future investigation dissecting the role of FAM26F in activation of various immune cell populations in local amplification by cell-cell contact is crucial to provide the missing link imperative for elucidating the relevance of this protein in immune responses.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"42 4","pages":"247-257"},"PeriodicalIF":5.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/08830185.2016.1206098","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9633157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T cells populate the skin to provide an effective immunosurveillance against external insults and to maintain tissue homeostasis. Most cutaneous T cells are αβ T cells, however, γδ T cells also exist although in much lower frequency. Different subsets of αβ T cells can be found in the skin, such as short-lived effector T cells, central memory T cells, effector memory T cells, and tissue-resident memory T cells. Their differential biology, function, and location provide an ample spectrum of immune responses in the skin. Foxp3+ memory regulatory T cells have a pivotal role in maintaining homeostasis in the skin and their dysregulation has been linked with different skin pathologies. The skin also contains populations of non-classical T cells, such as γδ T cells, NK T cells, and MR1-restricted T cells. Their role in skin homeostasis and response to pathogens has been well established in the past years, however, there is also growing evidence of their role in mediating allergic skin inflammation and promoting sensitization to allergens. In this review, we provide an updated overview on the different subsets of T cells that populate the skin with a specific focus on their role in allergic skin inflammation.
{"title":"Diversity of T cells in the skin: Novel insights.","authors":"Natalija Novak, Leticia Tordesillas, Beatriz Cabanillas","doi":"10.1080/08830185.2021.1985116","DOIUrl":"https://doi.org/10.1080/08830185.2021.1985116","url":null,"abstract":"<p><p>T cells populate the skin to provide an effective immunosurveillance against external insults and to maintain tissue homeostasis. Most cutaneous T cells are αβ T cells, however, γδ T cells also exist although in much lower frequency. Different subsets of αβ T cells can be found in the skin, such as short-lived effector T cells, central memory T cells, effector memory T cells, and tissue-resident memory T cells. Their differential biology, function, and location provide an ample spectrum of immune responses in the skin. Foxp3+ memory regulatory T cells have a pivotal role in maintaining homeostasis in the skin and their dysregulation has been linked with different skin pathologies. The skin also contains populations of non-classical T cells, such as γδ T cells, NK T cells, and MR1-restricted T cells. Their role in skin homeostasis and response to pathogens has been well established in the past years, however, there is also growing evidence of their role in mediating allergic skin inflammation and promoting sensitization to allergens. In this review, we provide an updated overview on the different subsets of T cells that populate the skin with a specific focus on their role in allergic skin inflammation.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"42 3","pages":"185-198"},"PeriodicalIF":5.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9447609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cardiovascular disease is the most common cause of death, which has the highest mortality rate worldwide. Although a diverse range of inflammatory diseases can affect the cardiovascular system, however, heart failure and stroke occur due to atherosclerosis. Atherosclerosis is a chronic autoinflammatory disease of small to large vessels in which different immune mediators are involved in lipid plaque formation and inflammatory vascular remodeling process. A better understanding of the pathophysiology of atherosclerosis may lead to uncovering immunomodulatory therapies. Despite present diagnostic and therapeutic methods, the lack of immunotherapy in the prevention and treatment of atherosclerosis is perceptible. In this review, we will discuss the promising immunological-based therapeutics and novel preventive approaches for atherosclerosis. This study could provide new insights into a better perception of targeted therapeutic pathways and biological therapies. [Formula: see text].
{"title":"The potential targets in immunotherapy of atherosclerosis.","authors":"Azin Aghamajidi, Melika Gorgani, Faezeh Shahba, Zahra Shafaghat, Nazanin Mojtabavi","doi":"10.1080/08830185.2021.1988591","DOIUrl":"https://doi.org/10.1080/08830185.2021.1988591","url":null,"abstract":"<p><p>Cardiovascular disease is the most common cause of death, which has the highest mortality rate worldwide. Although a diverse range of inflammatory diseases can affect the cardiovascular system, however, heart failure and stroke occur due to atherosclerosis. Atherosclerosis is a chronic autoinflammatory disease of small to large vessels in which different immune mediators are involved in lipid plaque formation and inflammatory vascular remodeling process. A better understanding of the pathophysiology of atherosclerosis may lead to uncovering immunomodulatory therapies. Despite present diagnostic and therapeutic methods, the lack of immunotherapy in the prevention and treatment of atherosclerosis is perceptible. In this review, we will discuss the promising immunological-based therapeutics and novel preventive approaches for atherosclerosis. This study could provide new insights into a better perception of targeted therapeutic pathways and biological therapies. [Formula: see text].</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"42 3","pages":"199-216"},"PeriodicalIF":5.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9454401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1080/08830185.2021.1960986
Divya Kandari, Rakesh Bhatnagar
As a natural function, antibodies defend the host from infected cells and pathogens by recognizing their pathogenic determinants. Antibodies (Abs) gained wide acceptance with an enormous impact on human health and have predominantly captured the arena of bio-therapeutics and bio-diagnostics. The scope of Ab-based biologics is vast, and it is likely to solve many unmet clinical needs in future. The majority of attention is now devoted to developing innovative technologies for manufacturing and engineering Abs, better suited to satisfy human needs. The advent of Ab engineering technologies (AET) led to phenomenal developments leading to the generation of Abs-/Ab-derived molecules with desirable functional properties proportional to their expanding requirements. Evolution brought by AET, from the naturally occurring Ab forms to several advanced Ab formats and derivatives, was much needed as it is of great interest to the pharmaceutical industry. Thus, numerous advancements in AET have propelled success in therapeutic Ab development, along with the potential for ever-increasing improvements. Unique characteristics of Abs, such as its diversity, specificity, structural integrity and an array of possible applications, together inspire continuous innovation in the field. Overall, the AET could assist in conquer of several limitations of Abs in terms of their applicability in the field of therapeutics, diagnostics and research; AET has so far led to the production of next-generation Abs, which have revolutionized these arenas. Here in this review, we discuss the various distinguished engineering platforms for Ab development and the progress in modern therapeutics by the so-called "next-generation Abs."
{"title":"Antibody engineering and its therapeutic applications.","authors":"Divya Kandari, Rakesh Bhatnagar","doi":"10.1080/08830185.2021.1960986","DOIUrl":"https://doi.org/10.1080/08830185.2021.1960986","url":null,"abstract":"<p><p>As a natural function, antibodies defend the host from infected cells and pathogens by recognizing their pathogenic determinants. Antibodies (Abs) gained wide acceptance with an enormous impact on human health and have predominantly captured the arena of bio-therapeutics and bio-diagnostics. The scope of Ab-based biologics is vast, and it is likely to solve many unmet clinical needs in future. The majority of attention is now devoted to developing innovative technologies for manufacturing and engineering Abs, better suited to satisfy human needs. The advent of Ab engineering technologies (AET) led to phenomenal developments leading to the generation of Abs-/Ab-derived molecules with desirable functional properties proportional to their expanding requirements. Evolution brought by AET, from the naturally occurring Ab forms to several advanced Ab formats and derivatives, was much needed as it is of great interest to the pharmaceutical industry. Thus, numerous advancements in AET have propelled success in therapeutic Ab development, along with the potential for ever-increasing improvements. Unique characteristics of Abs, such as its diversity, specificity, structural integrity and an array of possible applications, together inspire continuous innovation in the field. Overall, the AET could assist in conquer of several limitations of Abs in terms of their applicability in the field of therapeutics, diagnostics and research; AET has so far led to the production of next-generation Abs, which have revolutionized these arenas. Here in this review, we discuss the various distinguished engineering platforms for Ab development and the progress in modern therapeutics by the so-called \"next-generation Abs.\"</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"42 2","pages":"156-183"},"PeriodicalIF":5.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/08830185.2021.1960986","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9455709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1080/08830185.2022.2070616
Daisuke Ori, Taro Kawai
Inflammation plays indispensable roles in building the immune responses such as acquired immunity against harmful pathogens. Furthermore, it is essential for maintaining biological homeostasis in ever-changing conditions. Pattern-recognition receptors (PRRs) reside in cell membranes, endosomes or cytoplasm, and function as triggers for inflammatory responses. Binding of pathogen- or self-derived components, such as DNA, to PRRs activates downstream signaling cascades, resulting in the production of a series of pro-inflammatory cytokines and type I interferons (IFNs). While these series of responses are essential for host defense, the unexpected release of DNA from the nucleus or mitochondria of host cells can lead to autoimmune and autoinflammatory diseases. In this review, we focus on DNA-sensing mechanisms via PRRs and the disorders and extraordinary conditions caused by self-derived DNA.
{"title":"Pathophysiological functions of self-derived DNA.","authors":"Daisuke Ori, Taro Kawai","doi":"10.1080/08830185.2022.2070616","DOIUrl":"https://doi.org/10.1080/08830185.2022.2070616","url":null,"abstract":"<p><p>Inflammation plays indispensable roles in building the immune responses such as acquired immunity against harmful pathogens. Furthermore, it is essential for maintaining biological homeostasis in ever-changing conditions. Pattern-recognition receptors (PRRs) reside in cell membranes, endosomes or cytoplasm, and function as triggers for inflammatory responses. Binding of pathogen- or self-derived components, such as DNA, to PRRs activates downstream signaling cascades, resulting in the production of a series of pro-inflammatory cytokines and type I interferons (IFNs). While these series of responses are essential for host defense, the unexpected release of DNA from the nucleus or mitochondria of host cells can lead to autoimmune and autoinflammatory diseases. In this review, we focus on DNA-sensing mechanisms <i>via</i> PRRs and the disorders and extraordinary conditions caused by self-derived DNA.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"42 4","pages":"274-286"},"PeriodicalIF":5.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9578483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1080/08830185.2022.2095374
Keywan Mortezaee, Jamal Majidpoor
Metabolic reprogramming is a hallmark of solid cancers. Macrophages as major constituents of immune system take important roles in regulation of tumorigenesis. Pro-tumor M2 macrophages preferentially use oxidative phosphorylation (OXPHOS) to meet their metabolic demands, while anti-tumor M1 macrophages use glycolysis as their dominant metabolic source. Dysregulation in metabolic systems is a driving force of skewing macrophages from M1 toward M2 phenotypical state. Hyperactive M1 macrophages, for instance, release metabolic products that are contributed to M2 macrophage polarization. Thus, metabolic remodeling through reinstating normalization in metabolic systems can be an effective tool in cancer therapy. The key focus of this review is over metabolic systems in macrophages and factors influencing their metabolic acquisition and reprogramming in cancer, as well as discussing bout strategies to adjust macrophage metabolism and reeducation toward M1-like phenotype.
{"title":"Dysregulated metabolism: A friend-to-foe skewer of macrophages.","authors":"Keywan Mortezaee, Jamal Majidpoor","doi":"10.1080/08830185.2022.2095374","DOIUrl":"https://doi.org/10.1080/08830185.2022.2095374","url":null,"abstract":"<p><p>Metabolic reprogramming is a hallmark of solid cancers. Macrophages as major constituents of immune system take important roles in regulation of tumorigenesis. Pro-tumor M2 macrophages preferentially use oxidative phosphorylation (OXPHOS) to meet their metabolic demands, while anti-tumor M1 macrophages use glycolysis as their dominant metabolic source. Dysregulation in metabolic systems is a driving force of skewing macrophages from M1 toward M2 phenotypical state. Hyperactive M1 macrophages, for instance, release metabolic products that are contributed to M2 macrophage polarization. Thus, metabolic remodeling through reinstating normalization in metabolic systems can be an effective tool in cancer therapy. The key focus of this review is over metabolic systems in macrophages and factors influencing their metabolic acquisition and reprogramming in cancer, as well as discussing bout strategies to adjust macrophage metabolism and reeducation toward M1-like phenotype.</p>","PeriodicalId":14333,"journal":{"name":"International Reviews of Immunology","volume":"42 4","pages":"287-303"},"PeriodicalIF":5.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9633708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}