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Apoptosis and Its Relevance to Autoimmunity by Keith B. Elkon PDF

By Keith B. Elkon

ISBN-10: 3805580363

ISBN-13: 9783805580366

Over the past 15 years, apoptosis has turn into a dominant concentration of clinical study within the box of immunology. This book discusses the 3 significant parts of apoptosis learn: extrinsic dying receptor pathways, intrinsic telephone loss of life pathways and the mechanisms answerable for apoptotic telephone clearance. each one part delineates the proteins and sign transduction pathways and describes genetic adjustments that result in autoimmune ailments. even if such a lot mobilephone dying abnormalities were linked to systemic autoimmune problems resembling lupus erythematosus and lymphoproliferative syndromes, it truly is glaring that rules of telephone demise can also be pertinent to disorder expression in lots of organ-specific ailments akin to rheumatoid arthritis and glomerulonephritis.This quantity highlights the hot advances within the uncomplicated mechanisms of apoptosis and the appliance of that wisdom to realizing the effect of faulty apoptosis or faulty clearance of apoptotic cells at the immune functionality and the expression of ailment. it really is of detailed curiosity to cellphone biologists, immunologists and clinicians.

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Extra resources for Apoptosis and Its Relevance to Autoimmunity

Sample text

Wang J, Chun HJ, Wong W, Spencer DM, Lenardo MJ: Caspase-10 is an initiator caspase in death receptor signaling. Proc Natl Acad Sci USA 2001;98:13884–13888. Kischkel FC, Lawrence DA, Tinel A, et al: Death receptor recruitment of endogenous caspase-10 and apoptosis initiation in the absence of caspase-8. J Biol Chem 2001;276:46639–46646. Milhas D, Cuvillier O, Therville N, et al: Caspase-10 triggers bid cleavage and caspase cascade activation in FasL-induced apoptosis. J Biol Chem 2005;280:19836–19842.

The lpr strain carries a retrotransposon insertion within the fas gene, leading to an almost complete defect of Fas expression. It is proposed that lpr CD8ĪŠ T cells cannot be killed following stimulation by self-antigen. Consequently, they modulate the co-receptor, and accumulate as IL-10 secreting anergic cells [28, 29]. e. the lprcg and gld mice [30]. In the lprcg strain, a missense mutation within the Fas DD allows the expression of a nonfunctional protein. In the gld mouse, a missense mutation in the extracellular domain of FasL abrogates its interaction with Fas.

USA and from Koopman WJ: Apoptosis and autoimmune disease, chap 26,; in Mountz JD, Zhou T (eds): Arthritis and Allied Conditions, ed 15. Baltimore, Lippincott Williams & Wilkins). homology (BH1-4) domain regions, which control the ability of these proteins to dimerize and affect apoptosis. The conserved domains BH1, BH2, and BH3 participate in the formation of various dimer pairs as well as the regulation of cell death. The Bcl-2 family includes the death antagonists Bcl-2, Bcl-XL, Mcl-1, and A1, as well as the proapoptotic molecules Bax, Bcl-Xs, Bak, Bik, Bid, Bim, and Bad.

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Apoptosis and Its Relevance to Autoimmunity by Keith B. Elkon

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