By Sudhir Paul (auth.), Sudhir Paul (eds.)
Autoimmune Reactions tackles primary questions about how the immune approach can smash invading microbial pathogens with out inflicting harm to itself and different "self" structures. The authoritative specialists writing the following discover the mechanistic facets of such autoimmune ailments as lupus, rheumatoid arthritis, diabetes, and autoimmune thyroid affliction, and the place attainable delineate how malfunctioning immunological mechanisms may end up in medical indicators. in addition they talk about attainable normal mechanisms of autoimmune disease-e.g., molecular mimicry and dysfunctional antigen presentation-and their present barriers as unifying motives of the ailments defined. additionally, proof for novel immunological phenomena, together with antibody catalysis and the penetration of cells by means of antibodies, is reviewed, and their attainable organic effects are pointed out. The booklet additionally significantly surveys the techniques and learn that are supposed to ultimately enable improvement of palliatives and remedies for autoimmune ailments, in addition to methods to the long-standing challenge of self-nonself discrimination by means of the immune system.
the excellent, insightful assessment supplied in Autoimmune Reactions constitutes the recent commonplace reference for all practising autoimmunologists, molecular immunologists, mobile and molecular pathologists, and medical immunologists who have to stay on the state-of-the-art of analysis on autoimmune disorder this day.
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178, 1419-1428. 39. Pruzanski, W. and Shumak, K. H. (1977) Biologic activity of cold reacting autoantibodies. N. Eng!. 1. Med. 297,538-542. 40. , Kunkel, H. , and Mellors, R. C. (1961) Studies of a Waldenstrom-type macroglobulin with rheumatoid factor properties. 1. Lab. Clin. 57,905-912. 41. Crowley, J. , Goldfien, R. , Schrohenlober, R. , Spiegelberg, H. , Silverman, G. J, Mageed, R. A, et al. (1988) Incidence of three cross-reactive idiotypes on human rheumatoid factor paraproteins. 1. Immunol.
TPOAb are able to mediate ADCC, and unlike TGAb, they can also fix complement (84,85). ADCC is mediated by the interaction of NK cells with the Fe portion of the TPOAb that are in tum attached to TFC. Despite initial suggestions of more ADCC activity in PM compared to HT (82), a recent study was unable to find differences in ADCC activity between sera from patients with HT, PM, and GD (86). Terminal complement complexes (TCC), the fluid phase products released after formation of membrane attack complexes (MAC), surround the thyroid follicles in ATD, and their levels are elevated in patient sera, suggesting a major role for complement-mediated cell damage in ATD.
24) Dnuma et al. (25Y' 8adenhoop et al. (26) Population DR Caucasians Caucasians Caucasians DQBI 0301(M) Caucasians 81*0402 Japanese 81 *0501 Caucasians Caucasians Caucasians Protection Yanagawa et al. (23) Badenhoop et al. (26) Tarnai et al. (29) Cavan et al. (30) Caucasians Caucasians Japanese Chinese 0602 0501 0301 2. Hashimoto's thyroiditis Susceptibility 8adenhoop et al. (31) Tandon et al. (32) Shi et al. (33) Wu et al. (34) Santamaria et al. (35) Badenhoop et al. (26) Caucasians None Caucasians None Caucasians Caucasians None Caucasians Caucasians 0301(DQw7) 020 I (DQw2) 0201 0301 0201 0301 Japanese Caucasians 0602 0302 Cho et al.