By Sudhir Paul (auth.), Sudhir Paul (eds.)
Autoimmune Reactions tackles basic questions on how the immune procedure can smash invading microbial pathogens with no inflicting harm to itself and different "self" platforms. The authoritative specialists writing the following discover the mechanistic elements of such autoimmune illnesses as lupus, rheumatoid arthritis, diabetes, and autoimmune thyroid affliction, and the place attainable delineate how malfunctioning immunological mechanisms may end up in scientific indicators. in addition they talk about attainable normal mechanisms of autoimmune disease-e.g., molecular mimicry and dysfunctional antigen presentation-and their present obstacles as unifying causes of the ailments defined. furthermore, proof for novel immunological phenomena, together with antibody catalysis and the penetration of cells by means of antibodies, is reviewed, and their attainable organic results are pointed out. The e-book additionally significantly surveys the strategies and learn that are supposed to ultimately allow improvement of palliatives and therapies for autoimmune illnesses, in addition to ways to the long-standing challenge of self-nonself discrimination through the immune system.
the great, insightful review supplied in Autoimmune Reactions constitutes the recent common 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 sickness at the present time.
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Extra resources for Autoimmune Reactions
58) reported that 30% of CLL patients expressed the VH251 gene, which is one of the two germline sources of the VH5 gene family. Logtenberg et al. (59) found the heavy chains expressed in CLL B-Iymphocytes Autoimmunity and B-Cell Malignancies 25 to belong to the VH4 family in 50% of Igs, VH5 family in 20% and VH6 family in 15%. Further evidence for restricted VH gene use consists of the observation of the germinal VI-69 gene in 20% ofCLL cases (57). We studied VH family expression in 40 CD5+ B-CLL, and found VHl to be present in 17% of the Igs, VH2 in 8%, VH3 in 36%, VH4 in 17%, VH5 in 8%, and VH6 in 14% (60).
DNA and lysozyme), the transgenes are not deleted; they are simply down-regulated or anergized (25,26). These experiments throw light on the apparent discrepancy between Ehrlich, Landsteiner, and Metchnikoff. Indeed, the rule that a subject expressing the A or B blood group antigen will never produce autoantibodies against these determinants is widely accepted. We know of no cases of autoimmune hemolytic anemias displaying autoantibodies with this specificity. On the other hand, the production of autoantibodies against public antigens, like the I blood group antigen, is a common phenomenon (public antigens are defined here as nonpolymorphic conserved antigens shared by all members of a species).
55. , Binet, J. , and Dighiero, G. (1990) Evidence that chronic lymphocytic leukemia B lymphocytes are frequently committed to productions of natural autoantibodies. Blood 76, 562-569. 56. Kipps, T. , Chen, P. , and Carson, D. A. (1988) Autoantibody associated K light chain variable region gene expressed in chronic lymphocytic leukemia with little or no somatic mutation, implications for etiology and immunotherapy. J. Exp. Med. 167,840--852. 57. Kipps, T. , Pratt, L. , Chen, P. , and Carson, D.
Autoimmune Reactions by Sudhir Paul (auth.), Sudhir Paul (eds.)