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Book Chapter: B cell-mediated autoimmune diseases

TitleB cell-mediated autoimmune diseases
Authors
KeywordsAutoimmune diseases
B cell tolerance
Autoantibodies
Inflammatory cytokines
Issue Date2020
PublisherSpringer Nature
Citation
B cell-mediated autoimmune diseases. In Wang, J (Ed.), B Cells in Immunity and Tolerance, p. 145-160. Singapore: Springer Nature, 2020 How to Cite?
AbstractExtensive studies have suggested a central role of B cells in the autoimmune pathogenesis, as loss of B cell tolerance results in increased serum levels of autoantibodies, enhanced effector T cell response and tissue damages. Here, we provide an overview of dysregulated B cell responses in the development of autoimmunity. In addition to their presence in the target organs, autoreactive B cells can promote the formation of ectopic lymphoid structures and differentiate into plasma cells that produce large amounts of autoantibodies and cytokines. In animal models that recapitulate the key features of human autoimmune disease, mechanistic studies have indicated two categories of autoantibodies: (1) serological markers for disease diagnosis and prognosis; (2) effector molecules that induce organ hypofunction or damage directly in an epitope-specific manner, or indirectly by activating other immune cell subsets. Moreover, B cell-derived cytokines usually promote the autoreactive T cell response during autoimmune development, but there is compelling evidence that a subpopulation of B cells negatively regulates immune responses, also known as regulatory B cells via secreting anti-inflammatory cytokines (IL-10, IL-35, etc.) or a contact-dependent fashion. Although B cell depletion could eliminate most circulating B cells in the periphery, the clinical outcomes of B cell depletion therapy for autoimmune diseases vary among individuals due to differential activation or survival signals for B cells provided by tissue microenvironment. Thus, therapeutic combinations that target immune checkpoints and B cell activation may represent a promising strategy for the effective treatment of human autoimmune diseases.
Persistent Identifierhttp://hdl.handle.net/10722/284743
ISBN
Series/Report no.Advances in Experimental Medicine and Biology ; v. 1254

 

DC FieldValueLanguage
dc.contributor.authorLin, X-
dc.contributor.authorLu, L-
dc.date.accessioned2020-08-07T09:02:02Z-
dc.date.available2020-08-07T09:02:02Z-
dc.date.issued2020-
dc.identifier.citationB cell-mediated autoimmune diseases. In Wang, J (Ed.), B Cells in Immunity and Tolerance, p. 145-160. Singapore: Springer Nature, 2020-
dc.identifier.isbn9789811535314-
dc.identifier.urihttp://hdl.handle.net/10722/284743-
dc.description.abstractExtensive studies have suggested a central role of B cells in the autoimmune pathogenesis, as loss of B cell tolerance results in increased serum levels of autoantibodies, enhanced effector T cell response and tissue damages. Here, we provide an overview of dysregulated B cell responses in the development of autoimmunity. In addition to their presence in the target organs, autoreactive B cells can promote the formation of ectopic lymphoid structures and differentiate into plasma cells that produce large amounts of autoantibodies and cytokines. In animal models that recapitulate the key features of human autoimmune disease, mechanistic studies have indicated two categories of autoantibodies: (1) serological markers for disease diagnosis and prognosis; (2) effector molecules that induce organ hypofunction or damage directly in an epitope-specific manner, or indirectly by activating other immune cell subsets. Moreover, B cell-derived cytokines usually promote the autoreactive T cell response during autoimmune development, but there is compelling evidence that a subpopulation of B cells negatively regulates immune responses, also known as regulatory B cells via secreting anti-inflammatory cytokines (IL-10, IL-35, etc.) or a contact-dependent fashion. Although B cell depletion could eliminate most circulating B cells in the periphery, the clinical outcomes of B cell depletion therapy for autoimmune diseases vary among individuals due to differential activation or survival signals for B cells provided by tissue microenvironment. Thus, therapeutic combinations that target immune checkpoints and B cell activation may represent a promising strategy for the effective treatment of human autoimmune diseases.-
dc.languageeng-
dc.publisherSpringer Nature-
dc.relation.ispartofB Cells in Immunity and Tolerance-
dc.relation.ispartofseriesAdvances in Experimental Medicine and Biology ; v. 1254-
dc.subjectAutoimmune diseases-
dc.subjectB cell tolerance-
dc.subjectAutoantibodies-
dc.subjectInflammatory cytokines-
dc.titleB cell-mediated autoimmune diseases-
dc.typeBook_Chapter-
dc.identifier.emailLin, X: linxiang@hku.hk-
dc.identifier.emailLu, L: liweilu@hku.hk-
dc.identifier.authorityLin, X=rp02623-
dc.identifier.authorityLu, L=rp00477-
dc.identifier.doi10.1007/978-981-15-3532-1_11-
dc.identifier.scopuseid_2-s2.0-85083947431-
dc.identifier.hkuros311602-
dc.identifier.spage145-
dc.identifier.epage160-
dc.publisher.placeSingapore-

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