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

By Keith B. Elkon

Over the past 15 years, apoptosis has turn into a dominant concentration of scientific learn within the box of immunology. This ebook discusses the 3 significant parts of apoptosis examine: extrinsic loss of life receptor pathways, intrinsic telephone loss of life pathways and the mechanisms chargeable for apoptotic mobilephone clearance. each one part delineates the proteins and sign transduction pathways and describes genetic adjustments that result in autoimmune ailments. even though so much phone loss of life abnormalities were linked to systemic autoimmune problems similar to lupus erythematosus and lymphoproliferative syndromes, it's obvious that law of mobile demise is usually pertinent to sickness expression in lots of organ-specific illnesses corresponding to rheumatoid arthritis and glomerulonephritis.This quantity highlights the new advances within the simple mechanisms of apoptosis and the appliance of that wisdom to figuring out the impression of faulty apoptosis or faulty clearance of apoptotic cells at the immune functionality and the expression of ailment. it truly is of precise curiosity to mobile biologists, immunologists and clinicians.

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Immunity 1997;7:821–830. Pan G, Ni J, Wei YF, Yu G, Gentz R, Dixit VM: An antagonist decoy receptor and a death domaincontaining receptor for TRAIL [see comments]. Science 1997;277:815–818. Sheridan JP, Marsters SA, Pitti RM, et al: Control of TRAIL-induced apoptosis by a family of signaling and decoy receptors [see comments]. Science 1997;277:818–821. Schneider P, Thome M, Burns K, et al: TRAIL receptors 1 (DR4) and 2 (DR5) signal FADDdependent apoptosis and activate NF-␬B. Immunity 1997;7:831–836.

Adult MRL/lpr mice develop splenomegaly and adenopathy as well as hyperimmunoglobulinemia (hyper Ig), anti-nuclear antibody and nephritis. They accumulate CD4Ϫ, CD8Ϫ TCR ␣␤ϩ T cells called double-negative (DN) T cells in peripheral lymphoid organs. 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 CD8ϩ 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].

In contrast to lpr mice, typical lupus was never detected in Fas-deficient patients. ) Ag (1) DN T cellinduced TCR␣␤ DN T cells proliferation (sFasL, IL10) ALPS-Ia CD4+ or CD8+ T cells proliferation ALPS-Ia relatives Healthy carrier of a Fas mutation ->additional factors Fig. 4. Lymphoproliferation in ALPS-Ia and ALPS-Im. Fas-deficient cells (dark) and Fas-proficient cells (light), co-exist in ALPS-Im patients, showing the somatic mosaicism. In ALPS-Ia patients or in their clinically unaffected relatives, all cells are mutated and exhibit a Fas-mediated apoptosis defect.

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