V beta-dependent stimulation of bovine and human T cells by host-specific staphylococcal enterotoxins

被引:39
作者
Deringer, JR
Ely, RJ
Monday, SR
Stauffacher, CV
Bohach, GA
机构
[1] UNIV IDAHO,DEPT MICROBIOL MOL BIOL & BIOCHEM,MOSCOW,ID 83843
[2] PURDUE UNIV,DEPT BIOL SCI,W LAFAYETTE,IN 47907
关键词
D O I
10.1128/IAI.65.10.4048-4054.1997
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Staphylococcus aureus isolates from bovine and ovine species produce unique molecular variants of type C staphylococcal enterotoxin (SEC), The SEC animal variants have greater than 98% amino acid sequence identity with SEC1, a human-associated SEC, The two SEC animal variants have been designated SECbovine and SECovine according to their corresponding host species, We showed previously that these toxins induce quantitatively different levels of T-cell stimulation in several animal species. The present study compared the abilities of these closely related host-specific SEC variants to stimulate V beta-bearing T cells from bovine and human donors, All three toxins expanded human T cells bearing T-cell receptor V beta elements (huV beta) 3, 12, 13.2, 14, 15, 17, and 20, However, SEC1 resulted in greater expansion of hyV beta 12 than either SECbovine Or SECovine. In addition, bovine T cells proliferate in a V beta-dependent manner in response to these superantigens (SAgs), All three toxins induced the proliferation of bovine T cells bearing the previously sequenced V beta element (boV beta) from the bovine T-cell clone BTB13 (boV beta BTB13), SEC1 and SECovine also were able to induce proliferation of bovine T cells bearing boV beta BTB35, which SECbovine failed to stimulate. The species-specific differences in T-cell proliferation exhibited by these closely related SEC variants may reflect the evolutionary adaptation of S. aureus, presumably to increase its host range by the manipulation of the immune system in a host-specific manner.
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页码:4048 / 4054
页数:7
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