Chapter category: Autoimmunity
The Role of Cytokines as Effectors of Tissue Destruction in Autoimmunity
Cytokines and Chemokines in Autoimmune Disease
Edited by: Pere SantamariaISBN: 0-306-47693-2
» Get more information about this book at landesbioscience.com «
Chapter authors:
Thomas W.H. Kay, Rima Darwiche, Windy Irawaty, Mark M.W. Chong, Helen E. Thomas
Target cell damage in autoimmune disease is likely to be mediated by multiple effector pathways only some of which are cytokines. Recent progress in cell death research has dramatically changed ideas of how target cells might be destroyed and new effector pathways have been discovered. Multiple extra-cellular effector mechanisms may converge on a limited number of increasingly well-characterized intracellular cell death pathways. This increases the possibility that blockade of the damaging effects of inflammatory cytokines, cell death receptors that trigger caspase activation and noncytokine mechanisms such as the contents of the cytotoxic T cell granule may be a realistic and logical point of intervention in autoimmune disease.
Death of target cells is the culmination of the immunological events that cause many autoimmune diseases. When T cells specific for target cell autoantigens are activated they express a range of effector mechanisms analogous to those used by the immune system to clear infectious micro-organisms. The issue is to understand which are critical in target cell death in autoimmunity and how cells can be protected from them. This is a realistic and logical potential point of intervention.
Effector mechanisms of target organ damage have been most extensively studied in the pancreatic beta cell because of the realistic prospect of beta cell replacement therapy and the availability of many animal models of type 1 diabetes (T1DM). Beta cell destruction will therefore be the main focus of this review. Prospects for beta cell replacement as a treatment for T1DM have improved recently with progress in both islet cell transplantation1 and differentiation of pancreatic precursor cells2 or embryonal stem cells3 to insulin-producing cells4 Whatever forms of beta cell replacement are eventually most useful clinically they will require concurrent immunosuppression or, preferably, genetic modification for protection against the highly active anti-beta cell immune response found in people with established T1DM. A detailed knowledge of how beta cells are destroyed will indicate the most effective forms of immunoprotection and could eventually allow beta cell replacement without systemic immunosuppression. In other autoimmune diseases treatment with pharmacological replacement therapy is already successful (pernicious anemia, hypothyroidism) and knowledge of how target cells are killed is unlikely to be directly applied but is of scientific interest. In multiple sclerosis, replacement of damaged tissue seems unlikely in the short term but knowledge of mechanisms of disease may guide and refine systemic therapy.
Additional chapters from this book:
The Role of Cytokines as Effectors of Tissue Destruction in Autoimmunity
Thomas W.H. Kay, Rima Darwiche, Windy Irawaty, Mark M.W. Chong, Helen E. Thomas
Target cell damage in autoimmune disease is likely to be mediated by multiple effector pathways only some of which are cytokines. Recent progress in cell death research has dramatically cha...
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The Role of Cytokines as Effectors of Tissue Destruction in Autoimmunity
T Kay, R Darwiche, Wi Irawaty et al
Target cell damage in autoimmune disease is likely to be mediated by multiple effector pathways only some of which are cytokines. Recent progress in cell death research has dramatically change...
Cytokine and Cytokine Receptor Genes in the Susceptibility
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It is beyond the scope of this Chapter to review exhaustively the research on all autoimmune diseases. We will instead focus on three highly-prevalent chronic inflammat...
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Mark J. Cameron and David J. Kelvin
The immune system is skilled in communication and designed to respond quickly, specifically and globally to protect an organism against foreign invaders and disease. The cytokine superfamily o...
