Apoptosis and Its Relevance to Autoimmunity by Keith B. Elkon

By Keith B. Elkon

During the last 15 years, apoptosis has develop into a dominant concentration of clinical learn within the box of immunology. This e-book discusses the 3 significant components of apoptosis examine: extrinsic loss of life receptor pathways, intrinsic cellphone loss of life pathways and the mechanisms accountable for apoptotic mobilephone clearance. each one part delineates the proteins and sign transduction pathways and describes genetic changes that result in autoimmune illnesses. even though so much cellphone demise abnormalities were linked to systemic autoimmune issues comparable to lupus erythematosus and lymphoproliferative syndromes, it really is glaring that rules of mobile demise can also be pertinent to illness expression in lots of organ-specific illnesses akin to rheumatoid arthritis and glomerulonephritis.This quantity highlights the hot advances within the uncomplicated mechanisms of apoptosis and the applying of that wisdom to knowing the impression of faulty apoptosis or faulty clearance of apoptotic cells at the immune functionality and the expression of illness. it really is of targeted curiosity to cellphone biologists, immunologists and clinicians.

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Apoptosis and Its Relevance to Autoimmunity

Over the past 15 years, apoptosis has turn into a dominant concentration of clinical study within the box of immunology. This booklet discusses the 3 significant components of apoptosis learn: extrinsic dying receptor pathways, intrinsic phone dying pathways and the mechanisms liable for apoptotic mobilephone clearance.

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Cell 1995;81:935–946. Drappa J, Vaishnaw AK, Sullivan KE, Chu J-L, Elkon KB: Fas gene mutations in the CanaleSmith syndrome, an inherited lymphoproliferative disorder associated with autoimmunity. N Engl J Med 1996;335:1643–1649. Le Deist F, Emile JF, Rieux-Laucat F, et al: Clinical, immunological, and pathological consequences of Fas-deficient conditions. Lancet 1996;348:719–723. Genetic Bases of ALPS 33 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 Sneller MC, Wang J, Dale JK, et al: Clinical, immunologic, and genetic features of an autoimmune lymphoproliferative syndrome associated with abnormal lymphocyte apoptosis.

Human DN T cells are CD31ϩ but in contrast to recent thymic emigrants [53] they have a very low content of T cell recombination circle (TREC) [Rieux-Laucat, unpubl. data]. A striking feature of ALPS-Ia consists in overproduction of IL-10 by DN T cells along with reduced IL-12 production by monocytes [54]. This is likely a secondary regulatory event attempting to counterbalance the persistence and activation of autoimmune clones. This is consistent with the observation made in a mouse model where IL-10 was found to exacerbate autoimmune manifestations [29].

Bid and Bad possess the minimal death domain BH3, and the phosphorylation of Bad at Ser-112, Ser-136, and Ser-155 residue connects proximal survival signals to the Bcl-2 family. In contrast, the dephosphorylated (active) form of Bad binds to pro-survival Bcl-2 family members at the mitochondria. The binding of Bad to pro-survival Bcl-2 proteins is followed by the oligomerization of the proapoptotic Bcl-2 proteins Bax and Bak, which results in TNF Ligand-Receptor Superfamily and Arthritis 41 FasL-Fas FADD Caspase-8 (proximal caspases) Bid Bcl-2 Bcl-XL Cytochrome c/Apaf-1 Bax Bax Caspase-9 Apaf1 MIRT Caspase-3, -5 ,-7 (terminal caspases) p28Bap31 Bcl-2 Bcl-XL Apoptosis Bim Bad Inhibitors of apoptosis (IAPs) Fig.

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