V-BETA-DEPENDENT STIMULATION OF BOVINE AND HUMAN T-CELLS BY HOST-SPECIFIC STAPHYLOCOCCAL ENTEROTOXINS

Citation
Jr. Deringer et al., V-BETA-DEPENDENT STIMULATION OF BOVINE AND HUMAN T-CELLS BY HOST-SPECIFIC STAPHYLOCOCCAL ENTEROTOXINS, Infection and immunity, 65(10), 1997, pp. 4048-4054
Citations number
41
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
65
Issue
10
Year of publication
1997
Pages
4048 - 4054
Database
ISI
SICI code
0019-9567(1997)65:10<4048:VSOBAH>2.0.ZU;2-1
Abstract
Staphylococcus aureus isolates from bovine and ovine species produce u nique molecular variants of type C staphylococcal enterotoxin (SEC), T he SEC animal variants have greater than 98% amino acid sequence ident ity with SEC1, a human-associated SEC, The two SEC animal variants hav e been designated SECbovine and SECovine according to their correspond ing host species, We showed previously that these toxins induce quanti tatively different levels of T-cell stimulation in several animal spec ies. The present study compared the abilities of these closely related host-specific SEC variants to stimulate V beta-bearing T cells from b ovine and human donors, All three toxins expanded human T cells bearin g 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 tha n either SECbovine Or SECovine. In addition, bovine T cells proliferat e in a V beta-dependent manner in response to these superantigens (SAg s), All three toxins induced the proliferation of bovine T cells beari ng 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, whic h SECbovine failed to stimulate. The species-specific differences in T -cell proliferation exhibited by these closely related SEC variants ma y reflect the evolutionary adaptation of S. aureus, presumably to incr ease its host range by the manipulation of the immune system in a host -specific manner.