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The Role of Tumor Necrosis Factor Alpha in Autoimmunity (pp. 53-74) $100.00
Authors:  (Mariana Postal, Simone Appenzeller, Department of Medicine, Rheumatology Unit, Faculty of Medical Science, State University of Campinas, Brazil)
Abstract:
Cytokines are low-weight soluble proteins that are produced by
different cells in the innate and adaptive immune system. They mediate
activation or functional regulation of the immune system by binding to
cell surface receptors. They play a pivotal role in the differentiation,
maturation, and activation of various immune cells. The pleiotropic
cytokine tumor necrosis factor alpha (TNF-α) is a major participant in the
initiation and orchestration of complex events in inflammation and
immunity that produces different stimuli in various physiological and
pathological conditions. TNF-α contributes importantly to the
development of T cells, B cells, and dendritic cells. However, TNF-α is
also a potent inflammatory mediator and apoptosis inducer. The effects of
TNF-α are mediated by two structurally related, but functionally distinct
receptors, TNFR1 and TNFR2. These receptors also can be released from
the cell surface as soluble forms by proteolysis and have the capacity to neutralize the action of TNF-α. After binding TNFR1 or TNFR2, the
TNF-α signal transduction pathway is triggered. This complex
mechanism remais not completed understood. Futhermore, deregulated
TNF-α overexpression can give rise to chronic inflammatory and
autoimmune disorders, such as rheumatoid arthritis (RA), systemic lupus
erythematosus (SLE), and multiple sclerosis (MS). Currently, TNF-α
inhibitors are widely used and have shown encouraging results for the
treatment of these disorders. This chapter will give overview of the role
of TNF in autoimmunity, especially in autoimmune disorders, such as
rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and
multiple sclerosis (MS). 


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The Role of Tumor Necrosis Factor Alpha in Autoimmunity (pp. 53-74)