Apoptosis and Its Relevance to Autoimmunity by Keith B. Elkon

By Keith B. Elkon

During the last 15 years, apoptosis has turn into a dominant concentration of clinical examine within the box of immunology. This e-book discusses the 3 significant parts of apoptosis study: extrinsic dying receptor pathways, intrinsic telephone loss of life pathways and the mechanisms accountable for apoptotic mobile clearance. every one part delineates the proteins and sign transduction pathways and describes genetic changes that result in autoimmune ailments. even if such a lot cellphone loss of life abnormalities were linked to systemic autoimmune issues comparable to lupus erythematosus and lymphoproliferative syndromes, it truly is glaring that legislation of cellphone dying can be pertinent to illness expression in lots of organ-specific illnesses reminiscent of rheumatoid arthritis and glomerulonephritis.This quantity highlights the hot advances within the uncomplicated 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 illness. it truly is of specified curiosity to mobile biologists, immunologists and clinicians.

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Example text

Teachey DT, Manno CS, Axsom KM, et al: Unmasking Evans syndrome: T-cell phenotype and apoptotic response reveal autoimmune lymphoproliferative syndrome (ALPS). Blood 2005;105:2443–2448. Bader-Meunier B, Rieux-Laucat F, Croisille L, et al: Dyserythropoiesis associated with a fasdeficient condition in childhood. Br J Haematol 2000;108:300–304. Pensati L, Costanzo A, Ianni A, et al: Fas/Apo1 mutations and autoimmune lymphoproliferative syndrome in a patient with type 2 autoimmune hepatitis. Gastroenterology 1997;113: 1384–1389.

Cell 1997;89:1067–1076. Stanger B, Leder P, Lee T, Kim E, Seed B: RIP: A novel protein containing a death domain that interacts with fas/APO-1(CD95) in yeast and causes cell death. Cell 1995;81:513–523. Chu K, Niu X, Williams LT: A Fas-associated protein factor, FAF1, potentiates Fas-mediated apoptosis. Proc Natl Acad Sci USA 1995;92:11894–11898. Barnhart BC, Alappat EC, Peter ME: The CD95 type I/type II model. Semin Immunol 2003;15: 185–193. Siegel RM, Muppidi JR, Sarker M, et al: SPOTS: Signaling protein oligomeric transduction structures are early mediators of death receptor-induced apoptosis at the plasma membrane.

Pathophysiological Mechanisms in ALPS The characteristic feature of ALPS with Fas deficiency is chronic lymphoproliferation. The initial explanation was that Fas-deficient cells accumulate because of apoptosis resistance. However, if it fits with a progressive development of the disease in aging mice, it cannot explain the early onset of ALPS in children or in neonates. In addition, the frequent observation of spontaneous apoptosis of T cells in ALPS (either DN T cells or single positive CD4 or CD8) supports a dynamic generation/removal process of DN T cells.

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