Read e-book online Apoptosis and Its Relevance to Autoimmunity PDF

By Keith B. Elkon

ISBN-10: 3805580363

ISBN-13: 9783805580366

During the last 15 years, apoptosis has turn into a dominant concentration of clinical learn within the box of immunology. This e-book discusses the 3 significant parts of apoptosis study: extrinsic dying receptor pathways, intrinsic mobilephone loss of life pathways and the mechanisms chargeable for apoptotic cellphone clearance. every one part delineates the proteins and sign transduction pathways and describes genetic adjustments that result in autoimmune ailments. even supposing such a lot mobile loss of life abnormalities were linked to systemic autoimmune problems akin to lupus erythematosus and lymphoproliferative syndromes, it truly is glaring that legislation of telephone loss of life is usually pertinent to affliction expression in lots of organ-specific illnesses equivalent to rheumatoid arthritis and glomerulonephritis.This quantity highlights the hot advances within the easy mechanisms of apoptosis and the appliance of that wisdom to figuring out the influence of faulty apoptosis or faulty clearance of apoptotic cells at the immune functionality and the expression of illness. it truly is of detailed curiosity to mobilephone biologists, immunologists and clinicians.

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Extra resources for Apoptosis and Its Relevance to Autoimmunity

Sample text

However, as discussed below, somatic mutations of Fas, most likely occurring in hematopoietic progenitor, are also associated with classical benign ALPS [70]. Treatment indications depend on the type and severity of the symptoms. In many patients, the clinical status does not require any treatment. Splenectomy is often performed because of discomfort and hypersplenism. But sometimes it is also required because of protracted autoimmunity toward blood cells [50, 55]. In some patients autoimmunity tends to be severe, requiring aggressive immunosuppressive regimens including steroids and cyclophosphamide [49].

Chaudhary PM, Eby M, Jasmin A, Bookwalter A, Murray J, Hood L: Death receptor 5, a new member of the TNFR family, and DR4 induce FADD-dependent apoptosis and activate the NFkappaB pathway. 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].

Curr Dir Autoimmun. Basel, Karger, 2006, vol 9, pp 37–54 Tumor Necrosis Factor Ligand-Receptor Superfamily and Arthritis Hui-Chen Hsua, Yalei Wua, John D. , USA Abstract The current studies of apoptosis in rheumatoid arthritis (RA) suggest that the TNF ligand-receptor superfamily (TNFRsF) molecules, downstream pathways (activation of proapoptosis or anti-apoptosis pathway), cell types (lymphocytes and synovial fibroblast), and the mechanism that triggers apoptosis (tolerance induction-related, downmodulation of inflammation-related, or DNA damage-related) all exhibit a capability to determine the induction or prevention of RA.

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Apoptosis and Its Relevance to Autoimmunity by Keith B. Elkon

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