Pub Date : 2021-06-30DOI: 10.33696/immunology.3.092
K. Fiedorowicz, M. Kurpisz
Recently, stem/progenitor cell therapies have been intensively pursued. An increasing body of evidence has shown the promising results with respect to transient recovery of cardiac function in a variety of animal models with the use of stem cells interventions. Unfortunately, it is still not possible to fully and functionally replace the irreversibly damaged heart tissue. Moreover, the optimal cell population for organ regeneration has not been yet identified. Prior to possible optimization strategy to find ideal cell candidates, we shall keep in mind that successful organ regeneration is a very complex process. Within such development, the administered cells require proper homing and a graft retention that would be next followed by the cell electromechanical coupling with recipient organ cardiomyocytes [1]. Recent advances in molecular imaging techniques opened many platforms that would allow tracking of transplanted cells and optimization of delivery protocols with their subsequent multimodal imaging [2].
{"title":"Promoter Reporter Systems for Imaging of Cells Transplanted into Post-infarcted Heart","authors":"K. Fiedorowicz, M. Kurpisz","doi":"10.33696/immunology.3.092","DOIUrl":"https://doi.org/10.33696/immunology.3.092","url":null,"abstract":"Recently, stem/progenitor cell therapies have been intensively pursued. An increasing body of evidence has shown the promising results with respect to transient recovery of cardiac function in a variety of animal models with the use of stem cells interventions. Unfortunately, it is still not possible to fully and functionally replace the irreversibly damaged heart tissue. Moreover, the optimal cell population for organ regeneration has not been yet identified. Prior to possible optimization strategy to find ideal cell candidates, we shall keep in mind that successful organ regeneration is a very complex process. Within such development, the administered cells require proper homing and a graft retention that would be next followed by the cell electromechanical coupling with recipient organ cardiomyocytes [1]. Recent advances in molecular imaging techniques opened many platforms that would allow tracking of transplanted cells and optimization of delivery protocols with their subsequent multimodal imaging [2].","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49397988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.33696/immunology.3.082
Joseph B Moore, Marcin Wysoczynski
Myocardial infarction (MI) due to coronary artery stenosis compromises vascular endothelial integrity and increases vascular permeability [1,2]. Concurrently, ensuing myocardial tissue death and necrosis results in the release of danger associated molecular patterns (DAMPs), cytokines, chemokines, bioactive lipids, as well as activation of the complement cascade [1-3]. Collectively, these events direct a pronounced and immediate immune response, which includes the recruitment of peripheral blood leukocytes to the site of injury [2,3]. These infiltrating neutrophils are primarily responsible for the clearance of necrotic tissue and cellular debris in ischemic regions via their release of a host of proteolytic enzymes/proteases. While this constitutes a necessary early step in the myocardial repair process at the site of injury, neutrophil-derived reactive oxygen species (ROS) and pro-inflammatory cytokines/chemokines can contribute to collateral damage of surviving myocardium and amplify tissue injury [3,4]. Nevertheless, neutrophils are imperative for proper infarct healing as their depletion prior to MI leads to a dysregulated immune response, excessive scarring, and impaired ventricular function [5]. Within days of an MI, neutrophils undergo cell death and disappear from infarcted tissue [3,4]. Recruitment of neutrophils is followed by two waves of monocyte infiltration. First, early recruitment of Ly6CHigh monocytes expressing pro-inflammatory cytokines, and second, infiltration of Ly6CLow monocytes with pro-resolving and pro-reparative function [3,6,7]. Ly6CHigh monocyte migration is driven by the presence of tissue CCL2 chemokine gradients and their interaction with their cognate receptor, CCR2 [8]—a group of monocytes that are principally sourced from bone marrow and spleen. Subsequently, these monocytes differentiate into Ly6CLowCCR2High macrophages, known as monocyte-derived macrophages [9,10]. These are distinct from Ly6CLowCCR2Low macrophages deposited in the myocardial tissue during embryonic development [11-13]. Both macrophage populations (Ly6CLowCCR2High and Ly6CLowCCR2Low) contribute to myocardial repair by clearance of dead tissue via efferocytosis and production of pro-reparative and pro-resolving mediators. Macrophagederived cytokines play an essential role in the proliferation and activation of cardiac fibroblasts (fibroblast-myofibroblast conversion) that deposit collagen at the site of injury. This process of scar formation fulfills the immediate need to preserve the structural integrity
{"title":"Immunomodulatory Effects of Cell Therapy after Myocardial Infarction.","authors":"Joseph B Moore, Marcin Wysoczynski","doi":"10.33696/immunology.3.082","DOIUrl":"https://doi.org/10.33696/immunology.3.082","url":null,"abstract":"Myocardial infarction (MI) due to coronary artery stenosis compromises vascular endothelial integrity and increases vascular permeability [1,2]. Concurrently, ensuing myocardial tissue death and necrosis results in the release of danger associated molecular patterns (DAMPs), cytokines, chemokines, bioactive lipids, as well as activation of the complement cascade [1-3]. Collectively, these events direct a pronounced and immediate immune response, which includes the recruitment of peripheral blood leukocytes to the site of injury [2,3]. These infiltrating neutrophils are primarily responsible for the clearance of necrotic tissue and cellular debris in ischemic regions via their release of a host of proteolytic enzymes/proteases. While this constitutes a necessary early step in the myocardial repair process at the site of injury, neutrophil-derived reactive oxygen species (ROS) and pro-inflammatory cytokines/chemokines can contribute to collateral damage of surviving myocardium and amplify tissue injury [3,4]. Nevertheless, neutrophils are imperative for proper infarct healing as their depletion prior to MI leads to a dysregulated immune response, excessive scarring, and impaired ventricular function [5]. Within days of an MI, neutrophils undergo cell death and disappear from infarcted tissue [3,4]. Recruitment of neutrophils is followed by two waves of monocyte infiltration. First, early recruitment of Ly6CHigh monocytes expressing pro-inflammatory cytokines, and second, infiltration of Ly6CLow monocytes with pro-resolving and pro-reparative function [3,6,7]. Ly6CHigh monocyte migration is driven by the presence of tissue CCL2 chemokine gradients and their interaction with their cognate receptor, CCR2 [8]—a group of monocytes that are principally sourced from bone marrow and spleen. Subsequently, these monocytes differentiate into Ly6CLowCCR2High macrophages, known as monocyte-derived macrophages [9,10]. These are distinct from Ly6CLowCCR2Low macrophages deposited in the myocardial tissue during embryonic development [11-13]. Both macrophage populations (Ly6CLowCCR2High and Ly6CLowCCR2Low) contribute to myocardial repair by clearance of dead tissue via efferocytosis and production of pro-reparative and pro-resolving mediators. Macrophagederived cytokines play an essential role in the proliferation and activation of cardiac fibroblasts (fibroblast-myofibroblast conversion) that deposit collagen at the site of injury. This process of scar formation fulfills the immediate need to preserve the structural integrity","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"3 2","pages":"85-90"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8098722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38889821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.33696/immunology.3.090
Joshua S Mytych, Zijian Pan, A Darise Farris
Bacillus anthracis (Ba) is a gram-positive, rod-shaped, sporeand toxin-forming bacterium. While mainly an herbivore pathogen, human infection with Ba spores can occur through a number of routes including cutaneous, gastrointestinal, injectional, or inhalational [1]. The deadliest form of anthrax exposure is through inhalation of Ba spores, leading to systemic dissemination of the bacteria, with mortality ranging from 45% to 90% [2,3]. Current evidence suggests that sepsis, defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection [4], is likely to play a critical role in death from systemic anthrax [5].
{"title":"Efferocytosis and Anthrax: Implications for Bacterial Sepsis?","authors":"Joshua S Mytych, Zijian Pan, A Darise Farris","doi":"10.33696/immunology.3.090","DOIUrl":"https://doi.org/10.33696/immunology.3.090","url":null,"abstract":"Bacillus anthracis (Ba) is a gram-positive, rod-shaped, sporeand toxin-forming bacterium. While mainly an herbivore pathogen, human infection with Ba spores can occur through a number of routes including cutaneous, gastrointestinal, injectional, or inhalational [1]. The deadliest form of anthrax exposure is through inhalation of Ba spores, leading to systemic dissemination of the bacteria, with mortality ranging from 45% to 90% [2,3]. Current evidence suggests that sepsis, defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection [4], is likely to play a critical role in death from systemic anthrax [5].","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"3 3","pages":"133-139"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8547791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39565056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.33696/IMMUNOLOGY.3.079
B. Kassamali, A. J. Tan, Ellen B. Franciosi, M. Rashighi, A. Lachance
The COVID-19 pandemic has placed unprecedented strains on our medical system as specialties have had to reconsider “essential” in-person services and find novel ways to remotely ensure continuity of care. One such modality of care includes telehealth services, which have experienced a rapid rise in utility with a reported 4,347% increase in telehealth visits from March 2019 to March 2020 [1]. Although used for decades, telemedicine has historically been limited by reimbursement, as well as systems adoption and maintenance costs. Physical distancing measures throughout the pandemic, however, necessitated essentially overnight adoption of insurance coverage in both public and private sectors. Dermatology is among the earliest and most well-suited specialties to adopt telemedicine given the visual nature of the specialty [2]. Since the onset of the COVID-19 pandemic, we have seen a radical uptake of teledermatology services across the nation. In this paper, we review the literature published to date highlighting the state of teledermatology prior to the pandemic, the policy changes that facilitated the rapid expansion of teledermatology services during the pandemic, and the impact this has had on our dermatologic practices now and moving forward.
{"title":"Teledermatology Before, During, and After Covid-19: A Vital Tool to Improve Access and Equity in Specialty Care","authors":"B. Kassamali, A. J. Tan, Ellen B. Franciosi, M. Rashighi, A. Lachance","doi":"10.33696/IMMUNOLOGY.3.079","DOIUrl":"https://doi.org/10.33696/IMMUNOLOGY.3.079","url":null,"abstract":"The COVID-19 pandemic has placed unprecedented strains on our medical system as specialties have had to reconsider “essential” in-person services and find novel ways to remotely ensure continuity of care. One such modality of care includes telehealth services, which have experienced a rapid rise in utility with a reported 4,347% increase in telehealth visits from March 2019 to March 2020 [1]. Although used for decades, telemedicine has historically been limited by reimbursement, as well as systems adoption and maintenance costs. Physical distancing measures throughout the pandemic, however, necessitated essentially overnight adoption of insurance coverage in both public and private sectors. Dermatology is among the earliest and most well-suited specialties to adopt telemedicine given the visual nature of the specialty [2]. Since the onset of the COVID-19 pandemic, we have seen a radical uptake of teledermatology services across the nation. In this paper, we review the literature published to date highlighting the state of teledermatology prior to the pandemic, the policy changes that facilitated the rapid expansion of teledermatology services during the pandemic, and the impact this has had on our dermatologic practices now and moving forward.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69670783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.33696/immunology.3.073
Hiro Tatetsu, Daniel G Tenen, Li Chai
Currently, there is a growing need for culturing hematopoietic stem/progenitor cells (HSPCs) ex vivo for various clinical applications such as HSPC transplantation and gene therapy. For many patients with hematologic, genetic, and immune diseases, HSPC transplants can be a life-saving treatment. There are over 20,000 patients in the US receiving HSPC transplantation yearly [1]. About two-thirds of these cases are autologous and the rest are allogeneic transplants. The sources of the HSPCs are from peripheral blood mobilized stem/progenitor cells (PBSC), cord blood (CB) and bone marrow (BM). Umbilical cord blood can be an excellent HSPC donor source; however, its use is severely constrained by the limited HSPC numbers in one single cord blood unit. Developing technologies that allow ex vivo expansion of cord blood will be highly beneficial for the clinical application of HSPC transplants. In addition, there is a growing need for culturing PBSC in vitro for transplant-related applications such as gene therapy or genome-editing via TALENs or CRISPR/Cas9 [2,3]. Furthermore, the same PBSC in vitro culture technique can be used for HSCP expansion for poor autologous mobilizations to avoid additional collections. Establishing culture conditions that can maintain and expand HSPCs from PBSC ex vivo will be beneficial to these clinical applications.
{"title":"The Interplay between Transcription Factor SALL4 and Histone Modifiers in Hematopoietic Stem and Progenitor Cells.","authors":"Hiro Tatetsu, Daniel G Tenen, Li Chai","doi":"10.33696/immunology.3.073","DOIUrl":"https://doi.org/10.33696/immunology.3.073","url":null,"abstract":"Currently, there is a growing need for culturing hematopoietic stem/progenitor cells (HSPCs) ex vivo for various clinical applications such as HSPC transplantation and gene therapy. For many patients with hematologic, genetic, and immune diseases, HSPC transplants can be a life-saving treatment. There are over 20,000 patients in the US receiving HSPC transplantation yearly [1]. About two-thirds of these cases are autologous and the rest are allogeneic transplants. The sources of the HSPCs are from peripheral blood mobilized stem/progenitor cells (PBSC), cord blood (CB) and bone marrow (BM). Umbilical cord blood can be an excellent HSPC donor source; however, its use is severely constrained by the limited HSPC numbers in one single cord blood unit. Developing technologies that allow ex vivo expansion of cord blood will be highly beneficial for the clinical application of HSPC transplants. In addition, there is a growing need for culturing PBSC in vitro for transplant-related applications such as gene therapy or genome-editing via TALENs or CRISPR/Cas9 [2,3]. Furthermore, the same PBSC in vitro culture technique can be used for HSCP expansion for poor autologous mobilizations to avoid additional collections. Establishing culture conditions that can maintain and expand HSPCs from PBSC ex vivo will be beneficial to these clinical applications.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"3 1","pages":"26-30"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8057709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38897045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.33696/immunology.3.116
Suzana D Savkovic
Inflammatory Bowel Disease (IBD), which includes Crohn’s Disease (CD) and Ulcerative Colitis (UC), has a heterogeneous pathogenesis underlined by genetic predisposition, intestinal barrier dysfunction, impaired immune response, and microbiota imbalance [1-3]. This proceeds to aberrant immune cells presence and function in the affected tissue, activation of signaling pathways, and expression of regulators that subsequently drive inflammation [2,4-7]. Using publicly available transcriptomes obtained from large number of UC patients from European and the US cohorts [8-16], we identified systemic immune cell landscape, pathways, and transcriptional signatures specific for UC as well as those determining outcome of biologic therapy [17]. immune cell colonic cells, active
{"title":"Immune Cells and Transcriptional Signatures Revealed Novel Regulators and Predict Clinical Response to Biologic Therapy in Ulcerative Colitis.","authors":"Suzana D Savkovic","doi":"10.33696/immunology.3.116","DOIUrl":"https://doi.org/10.33696/immunology.3.116","url":null,"abstract":"Inflammatory Bowel Disease (IBD), which includes Crohn’s Disease (CD) and Ulcerative Colitis (UC), has a heterogeneous pathogenesis underlined by genetic predisposition, intestinal barrier dysfunction, impaired immune response, and microbiota imbalance [1-3]. This proceeds to aberrant immune cells presence and function in the affected tissue, activation of signaling pathways, and expression of regulators that subsequently drive inflammation [2,4-7]. Using publicly available transcriptomes obtained from large number of UC patients from European and the US cohorts [8-16], we identified systemic immune cell landscape, pathways, and transcriptional signatures specific for UC as well as those determining outcome of biologic therapy [17]. immune cell colonic cells, active","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":"343-347"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9431358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40344042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kae Myriam Pusic, Lisa Won, Richard Paul Kraig, Aya Darinka Pusic
Environmental enrichment produces beneficial effects in the brain at genetic, molecular, cellular and behavior levels, and has long been studied as a therapeutic intervention for a wide variety of neurological disorders. However, the complexity of applying a robust environmental enrichment paradigm makes clinical use difficult. Accordingly, there has been increased interest in developing environmental enrichment mimetics, also known as enviromimetics. Here we review the benefits of environmental enrichment for migraine treatment, and discuss the potential of using extracellular vesicles derived from interferon gamma-stimulated dendritic cells as an effective mimetic.
{"title":"Environmental Enrichment and Its Benefits for Migraine: Dendritic Cell Extracellular Vesicles as an Effective Mimetic.","authors":"Kae Myriam Pusic, Lisa Won, Richard Paul Kraig, Aya Darinka Pusic","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Environmental enrichment produces beneficial effects in the brain at genetic, molecular, cellular and behavior levels, and has long been studied as a therapeutic intervention for a wide variety of neurological disorders. However, the complexity of applying a robust environmental enrichment paradigm makes clinical use difficult. Accordingly, there has been increased interest in developing environmental enrichment mimetics, also known as enviromimetics. Here we review the benefits of environmental enrichment for migraine treatment, and discuss the potential of using extracellular vesicles derived from interferon gamma-stimulated dendritic cells as an effective mimetic.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"3 4","pages":"215-225"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8321388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39274864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.33696/immunology.3.076
Anas Alkhani, Sarah Mohamedaly, Amar Nijagal
Perinatal liver inflammation can have life-threatening consequences, particularly in infants and young children. An example of a hepatic inflammatory disease during infancy is biliary atresia (BA), an obliterative cholangiopathy that rapidly progresses to hepatic fibrosis and liver failure. The aggressive nature of BA in neonates compared to the pathogenesis of inflammatory liver diseases in adults, suggests that the mechanisms responsible for restoring tissue homeostasis following inflammation are impaired in affected infants. This article reviews our recent findings demonstrating that the relative abundance of Ly6cLo non-classical monocytes promotes resolution of perinatal liver injury in a murine model of perinatal hepatic inflammation. Our research also identifies a potential co-regulatory role between neutrophils and non-classical monocytes. Further work is needed to understand how neutrophils regulate other myeloid populations during perinatal liver inflammation. Elucidating the mechanisms that govern perinatal liver injury and repair may lead to the development of immune-directed therapies that can be used to mitigate the devastating effects of diseases like BA.
{"title":"The Role of Myeloid Populations during Perinatal Liver Injury and Repair.","authors":"Anas Alkhani, Sarah Mohamedaly, Amar Nijagal","doi":"10.33696/immunology.3.076","DOIUrl":"https://doi.org/10.33696/immunology.3.076","url":null,"abstract":"<p><p>Perinatal liver inflammation can have life-threatening consequences, particularly in infants and young children. An example of a hepatic inflammatory disease during infancy is biliary atresia (BA), an obliterative cholangiopathy that rapidly progresses to hepatic fibrosis and liver failure. The aggressive nature of BA in neonates compared to the pathogenesis of inflammatory liver diseases in adults, suggests that the mechanisms responsible for restoring tissue homeostasis following inflammation are impaired in affected infants. This article reviews our recent findings demonstrating that the relative abundance of Ly6c<sup>Lo</sup> non-classical monocytes promotes resolution of perinatal liver injury in a murine model of perinatal hepatic inflammation. Our research also identifies a potential co-regulatory role between neutrophils and non-classical monocytes. Further work is needed to understand how neutrophils regulate other myeloid populations during perinatal liver inflammation. Elucidating the mechanisms that govern perinatal liver injury and repair may lead to the development of immune-directed therapies that can be used to mitigate the devastating effects of diseases like BA.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"3 1","pages":"42-45"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9531850/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33488828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.33696/IMMUNOLOGY.3.075
S. Adam, G. Schett, S. Frey
Cytokine receptors may possess an intrinsic capability for the transduction of signals upon engagement by the respective cytokine ligand [1]. However, if they lack an own intracellular signaling entity, they rely on other signaling machineries. One of the key intracellular signaling molecules mediating cytokine effects on immune cells are Janus kinases (JAKs), which induce gene expression via signal transducer and activator of transcription proteins (STATs). In mammals, four JAK (JAK1, JAK2, JAK3 and Tyk2) and seven STAT proteins (STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B and STAT6) are described, which in varying combinations mediate signal transduction of well over fifty cytokines [2,3]. In the following article the role of JAK and STAT will be summarized.
{"title":"Prospects of JAK Inhibition in the Framework of Bone Loss","authors":"S. Adam, G. Schett, S. Frey","doi":"10.33696/IMMUNOLOGY.3.075","DOIUrl":"https://doi.org/10.33696/IMMUNOLOGY.3.075","url":null,"abstract":"Cytokine receptors may possess an intrinsic capability for the transduction of signals upon engagement by the respective cytokine ligand [1]. However, if they lack an own intracellular signaling entity, they rely on other signaling machineries. One of the key intracellular signaling molecules mediating cytokine effects on immune cells are Janus kinases (JAKs), which induce gene expression via signal transducer and activator of transcription proteins (STATs). In mammals, four JAK (JAK1, JAK2, JAK3 and Tyk2) and seven STAT proteins (STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B and STAT6) are described, which in varying combinations mediate signal transduction of well over fifty cytokines [2,3]. In the following article the role of JAK and STAT will be summarized.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69670738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.33696/immunology.3.099
Jason E Duex, Dan Theodorescu
Chemokines and their receptors are the communication mechanism used by cells of the immune system, allowing them to identify and eliminate pathogens and cancerous cells. However, it is becoming clear that chemokines and their receptors are also playing a role in tumor progression and metastasis [1,2]. An example of such coopting is the CCL2-CCR2 axis. The chemokine CCL2/MCP-1 (monocyte chemoattractant protein-1) is known to bind the CCR2 receptor on monocytes [3] and attract them to areas of need. What is now clear is that CCR2 levels are high in tumors of a number of cancer types. For example, in bladder cancer, 12 different patient datasets [4] all show that CCL2 expression is higher in the more advanced, muscle invasive disease than the non-muscle invasive disease [5]. In line with this, high CCL2 expression correlates with a worse overall survival in bladder cancer [5]. CCL2 and CCR2 are also associated with disease progression in many other cancer types including breast, ovarian, lung and colon [6,7].
{"title":"The Potential of Combination Therapies and Patient Stratification to Improve CCR2 Inhibition Therapeutics.","authors":"Jason E Duex, Dan Theodorescu","doi":"10.33696/immunology.3.099","DOIUrl":"https://doi.org/10.33696/immunology.3.099","url":null,"abstract":"Chemokines and their receptors are the communication mechanism used by cells of the immune system, allowing them to identify and eliminate pathogens and cancerous cells. However, it is becoming clear that chemokines and their receptors are also playing a role in tumor progression and metastasis [1,2]. An example of such coopting is the CCL2-CCR2 axis. The chemokine CCL2/MCP-1 (monocyte chemoattractant protein-1) is known to bind the CCR2 receptor on monocytes [3] and attract them to areas of need. What is now clear is that CCR2 levels are high in tumors of a number of cancer types. For example, in bladder cancer, 12 different patient datasets [4] all show that CCL2 expression is higher in the more advanced, muscle invasive disease than the non-muscle invasive disease [5]. In line with this, high CCL2 expression correlates with a worse overall survival in bladder cancer [5]. CCL2 and CCR2 are also associated with disease progression in many other cancer types including breast, ovarian, lung and colon [6,7].","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"3 3","pages":"198-200"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/05/fd/nihms-1724849.PMC8788950.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39739652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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