title: Genomic composition and allelic polymorphisms influence V beta usage by the Mycoplasma arthritidis superantigen.
abstract: The Mycoplasma arthritidis superantigen (MAM) is produced by an organism that causes systemic disease in rodents leading to chronic proliferative arthritis. MAM is a typical superantigen that requires presentation to T cells by MHC molecules without processing and T cell recognition of MAM occurs through the V beta chains of the TCR. Several major findings are presented here. First, different MAM-MHC class II isotype complexes may engage different sets of V beta TCR. Thus, activation of V beta 6- and V beta 8.3-bearing T cells is more dependent upon the I-E molecule of the murine H-2 MHC than is activation of cells bearing the V beta 5.1, 8.1, and 8.2 TCR. Secondly, both genomic composition and allelic polymorphisms at the V beta chain segment of the TCR exert profound effects upon the pattern of V beta that are used by MAM. Thus, in V beta b haplotype mice, MAM engages V beta 5.1, 6, and the V beta 8 family of TCR whereas in V beta a (C57BR) and V beta c (RIIIS) haplotype mice that lack various combinations of these V beta, activation of cells bearing V beta 1, 3.1, 7, and 16 can be demonstrated. These differences in V beta usage by MAM appear to be caused by both differences in the avidity of MAM for the various V beta s and to structural allelic polymorphisms in these V beta. Clonal expansion of specific V beta in vivo after injection of MAM is also dependent upon the genomic composition of the mice, because expansion of the V beta 8 TCR seen in V beta b haplotype mice (B10.RIII) whereas marked expansion of V beta 6 is seen in V beta a mice (C57BR). In as much as these TCR have been implicated in a number of experimental autoimmune diseases, MAM may represent an ideal model to evaluate the role of superantigens in the triggering of autoimmune disease.
authors: Division of Rheumatology, University of Utah School of Medicine, Salt Lake City 84132.
authors: B C
authors: BC
authors: Cole
authors: R A
authors: RA
authors: Balderas
authors: E A
authors: EA
authors: Ahmed
authors: D
authors: D
authors: Kono
authors: A N
authors: AN
authors: Theofilopoulos
mesh_terms: D000483:Alleles; D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology*; D001170:Arthritis, Infectious / Q000209:etiology; D006183:H-2 Antigens / Q000502:physiology; D006239:Haplotypes; D006801:Humans; D051379:Mice; D008809:Mice, Inbred C3H; D008808:Mice, Inbred CBA; D009174:Mycoplasma / Q000276:immunology*; D011110:Polymorphism, Genetic; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics*
chemical_list: D000942:Antigens, Bacterial; D006183:H-2 Antigens; D016693:Receptors, Antigen, T-Cell, alpha-beta