Pub Date : 2020-06-29DOI: 10.5772/intechopen.93005
Roxana Rodrígez-Barrera, Adrián Flores-Romero, J. García-Sánchez, L. Navarro-Torres, Marcela Garibay-López, Elisa García-Vences
The inflammatory response after a spinal cord injury (SCI) is a secondary mechanism of damage, this involves alterations at the local and systemic level, and it is mediated by cytokine participation that takes part actively. The excessive inflammatory response causes an autoreactive response that targets against components of the nervous tissue; this response lengthens the inflammatory process initiated during the acute phase. The participation of immune cells in acute phases is characterized by the arrival of neutrophils, macrophages, and microglia, as well as T lymphocytes, which express their peaks on different days post-injury (1st, 3rd, and 11th respectively). The chronic phase of the injury begins 14 days after it occurred, reaching its highest point at 60 days, and can still be detected the following 180 days. One of the outcomes of the inflammatory process and cytokine synthesis is the generation of glial scar. In this chapter, we will review the different cytokine mechanisms involved in the formation of glial scar in acute and chronic phases, as well as the modulating treatments of glial scar.
{"title":"Cytokines in Scar Glial Formation after an Acute and Chronic Spinal Cord Injury","authors":"Roxana Rodrígez-Barrera, Adrián Flores-Romero, J. García-Sánchez, L. Navarro-Torres, Marcela Garibay-López, Elisa García-Vences","doi":"10.5772/intechopen.93005","DOIUrl":"https://doi.org/10.5772/intechopen.93005","url":null,"abstract":"The inflammatory response after a spinal cord injury (SCI) is a secondary mechanism of damage, this involves alterations at the local and systemic level, and it is mediated by cytokine participation that takes part actively. The excessive inflammatory response causes an autoreactive response that targets against components of the nervous tissue; this response lengthens the inflammatory process initiated during the acute phase. The participation of immune cells in acute phases is characterized by the arrival of neutrophils, macrophages, and microglia, as well as T lymphocytes, which express their peaks on different days post-injury (1st, 3rd, and 11th respectively). The chronic phase of the injury begins 14 days after it occurred, reaching its highest point at 60 days, and can still be detected the following 180 days. One of the outcomes of the inflammatory process and cytokine synthesis is the generation of glial scar. In this chapter, we will review the different cytokine mechanisms involved in the formation of glial scar in acute and chronic phases, as well as the modulating treatments of glial scar.","PeriodicalId":77093,"journal":{"name":"Cytokines","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5772/intechopen.93005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41336004","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 : 2020-06-23DOI: 10.5772/intechopen.93004
Chantel F. Faqua, R. Akomeah, S. Adunyah
Interleukin-21 (IL-21) is produced by activated T cells and it plays many diverse roles by regulating the functions of normal and abnormal cells. Its roles include regulation of proliferation, promotion of immune system and activation of apoptosis in B cells. IL-21R is a type-1 cytokine receptor and belongs to the IL-2R and IL-15R family. The signaling mechanisms of IL-21 in different cell types have been identified. However, we know less about the biological effects of IL-21 and its signaling mechanisms in leukemia cells and monocytes. In this chapter, we will focus on IL-21’s biological effects and signaling pathways as well as discuss the potential implications and applications of IL-21 in leukemia cells. In these cells, IL-21 does not promote proliferation but enhances apoptosis and chemotaxis. Furthermore, IL-21 promotes differential expression of many cytokines including interleukins and chemokines. IL-21 activates both the Raf-ERK-MAPK and the Jak/STAT signaling pathways. These pathways mediate some of the effects of IL-21. Lastly, IL-21 also promotes activation of the STAT3 promoter and other transcriptional factors. These findings may be relevant to IL-21’s potential clinical implications and applications. in leukemia cells. Our results show that IL-21 activates Jak2, Jak 3 and Tyk2, which are involved in activating several STAT proteins including STAT2, STAT3, STAT4 and STAT6 in both U937 leukemia
{"title":"IL-21 Signaling and Induction of Cytokine Expression in Human Leukemia Cells and Monocytes","authors":"Chantel F. Faqua, R. Akomeah, S. Adunyah","doi":"10.5772/intechopen.93004","DOIUrl":"https://doi.org/10.5772/intechopen.93004","url":null,"abstract":"Interleukin-21 (IL-21) is produced by activated T cells and it plays many diverse roles by regulating the functions of normal and abnormal cells. Its roles include regulation of proliferation, promotion of immune system and activation of apoptosis in B cells. IL-21R is a type-1 cytokine receptor and belongs to the IL-2R and IL-15R family. The signaling mechanisms of IL-21 in different cell types have been identified. However, we know less about the biological effects of IL-21 and its signaling mechanisms in leukemia cells and monocytes. In this chapter, we will focus on IL-21’s biological effects and signaling pathways as well as discuss the potential implications and applications of IL-21 in leukemia cells. In these cells, IL-21 does not promote proliferation but enhances apoptosis and chemotaxis. Furthermore, IL-21 promotes differential expression of many cytokines including interleukins and chemokines. IL-21 activates both the Raf-ERK-MAPK and the Jak/STAT signaling pathways. These pathways mediate some of the effects of IL-21. Lastly, IL-21 also promotes activation of the STAT3 promoter and other transcriptional factors. These findings may be relevant to IL-21’s potential clinical implications and applications. in leukemia cells. Our results show that IL-21 activates Jak2, Jak 3 and Tyk2, which are involved in activating several STAT proteins including STAT2, STAT3, STAT4 and STAT6 in both U937 leukemia","PeriodicalId":77093,"journal":{"name":"Cytokines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5772/intechopen.93004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49080097","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 : 2019-12-13DOI: 10.5772/intechopen.85476
Mubarak Muhammad
Tumor necrosis factor (TNF) is one of the most extensively studied cytokine with about 19 distinct superfamily members and many more to be found. Prominent among these members is tumor necrosis factor alpha (TNF- α ) that is known to be a potent promoter of inflammation, as well as many normal physiological functions in homeostasis and health and antimicrobial immunity. Nuclear factor kappa-light-chain enhancer of activated B cells (NF κ B) is one of the most important transcription factors that activate transcription of many proinflammatory genes, and the unraveling of TNF- α induced NF κ B activation forms the foundation of TNF- α as major cytokine of neuroinflammation. This review discusses summary of literature on unique role of TNF- α in neuroinflammation and various agents that mediate neuroinflammation via TNF- α modulation.
{"title":"Tumor Necrosis Factor Alpha: A Major Cytokine of Brain Neuroinflammation","authors":"Mubarak Muhammad","doi":"10.5772/intechopen.85476","DOIUrl":"https://doi.org/10.5772/intechopen.85476","url":null,"abstract":"Tumor necrosis factor (TNF) is one of the most extensively studied cytokine with about 19 distinct superfamily members and many more to be found. Prominent among these members is tumor necrosis factor alpha (TNF- α ) that is known to be a potent promoter of inflammation, as well as many normal physiological functions in homeostasis and health and antimicrobial immunity. Nuclear factor kappa-light-chain enhancer of activated B cells (NF κ B) is one of the most important transcription factors that activate transcription of many proinflammatory genes, and the unraveling of TNF- α induced NF κ B activation forms the foundation of TNF- α as major cytokine of neuroinflammation. This review discusses summary of literature on unique role of TNF- α in neuroinflammation and various agents that mediate neuroinflammation via TNF- α modulation.","PeriodicalId":77093,"journal":{"name":"Cytokines","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5772/intechopen.85476","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41787626","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 : 2019-10-02DOI: 10.5772/intechopen.88856
A. A. Asmari, Misbahul Arfin
Behçet’s disease (BD) is a complex, multisystemic inflammatory disorder characterized by recurrent oral aphthous ulcers, ocular symptoms, skin lesions, and genital ulcerations. The etiology of BD is not yet clear though various factors including environmental, genetic and immunological ones have been implicated. Genetic predisposition is a major factor in disease susceptibility and multiple host genetic factors have been suggested to be involved in the development of BD. In addition to the positive association of HLAB*51, recent studies report additional independent associations in the non HLA loci. Single nucleotide polymorphisms (SNPs) in various genes including cytokines have been implicated in susceptibility to BD. However, the results are inconsistent and variation are found in several ethnic populations. Therefore, further genetic studies on BD patients of different ethnicity and genes associated with immunity are expected to elucidate BD pathogenesis and will contribute to the development of more targeted therapies and biomarkers.
{"title":"The Genetic Aspects of Behçet’s Disease: Role of Cytokine Genes Polymorphisms","authors":"A. A. Asmari, Misbahul Arfin","doi":"10.5772/intechopen.88856","DOIUrl":"https://doi.org/10.5772/intechopen.88856","url":null,"abstract":"Behçet’s disease (BD) is a complex, multisystemic inflammatory disorder characterized by recurrent oral aphthous ulcers, ocular symptoms, skin lesions, and genital ulcerations. The etiology of BD is not yet clear though various factors including environmental, genetic and immunological ones have been implicated. Genetic predisposition is a major factor in disease susceptibility and multiple host genetic factors have been suggested to be involved in the development of BD. In addition to the positive association of HLAB*51, recent studies report additional independent associations in the non HLA loci. Single nucleotide polymorphisms (SNPs) in various genes including cytokines have been implicated in susceptibility to BD. However, the results are inconsistent and variation are found in several ethnic populations. Therefore, further genetic studies on BD patients of different ethnicity and genes associated with immunity are expected to elucidate BD pathogenesis and will contribute to the development of more targeted therapies and biomarkers.","PeriodicalId":77093,"journal":{"name":"Cytokines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44448015","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 : 2019-07-04DOI: 10.5772/INTECHOPEN.87167
H. Jyonouchi
The neuroimmune network represents a dense network of multiple signals mediated by neurotransmitters, hormones, growth factors, and cytokines produced by multiple lineage cells and is crucial for maintaining neuroimmune homeostasis. Endogenous and exogenous stimuli, which are dangerous to the body, are detected by sensor cells, and they rapidly inform the brain through this network. Innate immunity is thought to play a major role in the neuroimmune network, through cytokines and other mediators released from secretary innate immune cells. Recent research has revealed that innate immunity has its own memory. This is accomplished by metabolic and epigenetic changes. Such changes may result in augmenting immune protection with a risk of excessive inflammatory responses to subsequent stimuli (trained immunity). Alternatively, innate immune memory can induce suppressive effects (tolerance), which may impose a risk of impaired immune defense. Innate immune memory affects the neuroimmune network for a prolonged period, and dysregulated innate immune memory has been implicated with pathogenesis of neuropsychiatric conditions. This chapter summarizes a role of innate immune memory (trained immunity vs. tolerance) in neuroinflammation in association with neuropsychiatric conditions including autism spectrum disorders (ASD).
{"title":"Innate Immunity and Neuroinflammation in Neuropsychiatric Conditions Including Autism Spectrum Disorders: Role of Innate Immune Memory","authors":"H. Jyonouchi","doi":"10.5772/INTECHOPEN.87167","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.87167","url":null,"abstract":"The neuroimmune network represents a dense network of multiple signals mediated by neurotransmitters, hormones, growth factors, and cytokines produced by multiple lineage cells and is crucial for maintaining neuroimmune homeostasis. Endogenous and exogenous stimuli, which are dangerous to the body, are detected by sensor cells, and they rapidly inform the brain through this network. Innate immunity is thought to play a major role in the neuroimmune network, through cytokines and other mediators released from secretary innate immune cells. Recent research has revealed that innate immunity has its own memory. This is accomplished by metabolic and epigenetic changes. Such changes may result in augmenting immune protection with a risk of excessive inflammatory responses to subsequent stimuli (trained immunity). Alternatively, innate immune memory can induce suppressive effects (tolerance), which may impose a risk of impaired immune defense. Innate immune memory affects the neuroimmune network for a prolonged period, and dysregulated innate immune memory has been implicated with pathogenesis of neuropsychiatric conditions. This chapter summarizes a role of innate immune memory (trained immunity vs. tolerance) in neuroinflammation in association with neuropsychiatric conditions including autism spectrum disorders (ASD).","PeriodicalId":77093,"journal":{"name":"Cytokines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5772/INTECHOPEN.87167","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42846030","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 : 2019-04-08DOI: 10.5772/INTECHOPEN.85632
Xuehui He, Xinhui Wang
TNF has both proinflammatory and antiinflammatory effects. It binds to two structurally related but functionally distinct receptors TNFR1 and TNFR2. Unlike TNFR1 that is ubiquitously expressed, TNFR2 expression is more limited to myeloid and lymphoid cell lineages including a fraction of regulatory T cells (Treg). In general, TNFR1 is responsible for TNF-mediated cell apoptosis and death, and mostly induces proinflammatory reactions. However, TNFR2 mainly leads to functions related to cell survival and immune suppression. Treg play an indispensable role in maintaining immunological self-tolerance and restraining excessive immune reactions deleterious to the host. Impaired Treg-mediated immune regulation has been observed in various autoimmune diseases as well as in cancers. Therefore, Treg might provide an ideal therapeutic target for diseases where the immune balance is impaired and could benefit from the regulation of Treg properties. TNFR2 is highly expressed on Treg in mice and in humans, and TNFR2+ Treg reveal the most potent suppressive capacity. TNF-TNFR2 ligation benefits Treg proliferation, although the effect on Treg suppressive function remains controversial. Here, we will describe in detail the TNF-mediated regulation of Treg and the potential clinical applications in cancer immunotherapy as well as in autoimmune diseases, with the focus on human Treg subsets.
{"title":"TNFR2 and Regulatory T Cells: Potential Immune Checkpoint Target in Cancer Immunotherapy","authors":"Xuehui He, Xinhui Wang","doi":"10.5772/INTECHOPEN.85632","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.85632","url":null,"abstract":"TNF has both proinflammatory and antiinflammatory effects. It binds to two structurally related but functionally distinct receptors TNFR1 and TNFR2. Unlike TNFR1 that is ubiquitously expressed, TNFR2 expression is more limited to myeloid and lymphoid cell lineages including a fraction of regulatory T cells (Treg). In general, TNFR1 is responsible for TNF-mediated cell apoptosis and death, and mostly induces proinflammatory reactions. However, TNFR2 mainly leads to functions related to cell survival and immune suppression. Treg play an indispensable role in maintaining immunological self-tolerance and restraining excessive immune reactions deleterious to the host. Impaired Treg-mediated immune regulation has been observed in various autoimmune diseases as well as in cancers. Therefore, Treg might provide an ideal therapeutic target for diseases where the immune balance is impaired and could benefit from the regulation of Treg properties. TNFR2 is highly expressed on Treg in mice and in humans, and TNFR2+ Treg reveal the most potent suppressive capacity. TNF-TNFR2 ligation benefits Treg proliferation, although the effect on Treg suppressive function remains controversial. Here, we will describe in detail the TNF-mediated regulation of Treg and the potential clinical applications in cancer immunotherapy as well as in autoimmune diseases, with the focus on human Treg subsets.","PeriodicalId":77093,"journal":{"name":"Cytokines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5772/INTECHOPEN.85632","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45780693","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 : 2019-03-25DOI: 10.5772/INTECHOPEN.85237
Sara Žigon-Branc, A. Barlič, M. Jeras
Human cell-based assays for in vitro testing of drugs in preclinical and research studies, as well as in clinical practice, are gaining greater importance especially in view of personalized medicine, which is tailored to the individual needs and benefits of a patient. This chapter begins with an overview of contemporary cell-based assays, routinely used for a comparative in vitro potency testing of anti-TNF- α innovator biologics and their biosimilars. In sequel, based on the results of our original work, we will further discuss the establishment and use of 2D normal and osteoarthritic primary chondrocyte monolayer cultures and 3D microspheroidal articular cartilage tissues, prepared in hanging drops from osteoarthritic chondrocytes and chondrogenically differentiated mesenchymal stem cells. Both 2D and 3D cultures will be presented as models for assessing the neutralizing potency of the three well-known anti-TNF- α biological drugs: adalimumab, etanercept, and infliximab.
{"title":"In vitro Cell-Based Assays for Potency Testing of Anti-TNF-α Biological Drugs","authors":"Sara Žigon-Branc, A. Barlič, M. Jeras","doi":"10.5772/INTECHOPEN.85237","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.85237","url":null,"abstract":"Human cell-based assays for in vitro testing of drugs in preclinical and research studies, as well as in clinical practice, are gaining greater importance especially in view of personalized medicine, which is tailored to the individual needs and benefits of a patient. This chapter begins with an overview of contemporary cell-based assays, routinely used for a comparative in vitro potency testing of anti-TNF- α innovator biologics and their biosimilars. In sequel, based on the results of our original work, we will further discuss the establishment and use of 2D normal and osteoarthritic primary chondrocyte monolayer cultures and 3D microspheroidal articular cartilage tissues, prepared in hanging drops from osteoarthritic chondrocytes and chondrogenically differentiated mesenchymal stem cells. Both 2D and 3D cultures will be presented as models for assessing the neutralizing potency of the three well-known anti-TNF- α biological drugs: adalimumab, etanercept, and infliximab.","PeriodicalId":77093,"journal":{"name":"Cytokines","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5772/INTECHOPEN.85237","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42847947","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}
{"title":"Generation of NAP-1 and related peptides in psoriasis and other inflammatory skin diseases.","authors":"J M Schröder","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77093,"journal":{"name":"Cytokines","volume":"4 ","pages":"54-76"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12643483","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 : 1992-01-01DOI: 10.1007/978-3-642-77405-8_75
A. Walz
{"title":"Generation and properties of neutrophil-activating peptide 2.","authors":"A. Walz","doi":"10.1007/978-3-642-77405-8_75","DOIUrl":"https://doi.org/10.1007/978-3-642-77405-8_75","url":null,"abstract":"","PeriodicalId":77093,"journal":{"name":"Cytokines","volume":"4 1","pages":"77-95"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51126923","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}
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