The Journal of Immunology, Vol 150, Issue 12 5231-5240, Copyright © 1993 by American Association of Immunologists

ARTICLES

Dissection of the function of HLA class II and costimulation in B cell- mediated and toxic shock syndrome toxin-1-induced T cell proliferation

D Dennig and RJ O'Reilly
Sloan-Kettering Institute, Department of Pediatrics, New York, NY.

In this study we have demonstrated that costimulation for TSST-1- induced T cell proliferation is provided by HLA class II negative accessory B cells. In addition, TSST-1 binding to these HLA class II negative accessory B cells could not be detected by immunocytofluorescence, or in a system in which T cell proliferation depended on TSST-1 pretreated HLA class II negative B cells. These findings suggest that accessory signals can be supplied by B cells that are not involved in the activation of T cells via Ag-HLA/TCR-CD3 complex interaction: TCR ligation by a TSST-1/HLA complex and costimulation need not be delivered by the same cell. In the presence of HLA class II negative B cells, T cell proliferation in response to TSST-1 could be achieved despite addition of a mAb that can block HLA class II binding sites for TSST-1. These findings suggest the possibility that TSST-1 may directly ligate TCR. In the presence of anti-BB1-treated HLA class II negative accessory cells, TSST-1-induced T cell proliferation was inhibited by over 50% indicating the involvement of the BB1/CD28 pathway. The leukemic pre-B cell lines NALM- 6, and BLIN-1, both of which express surface HLA class II Ag, but not the costimulatory B cell activation Ag BB1, were deficient in their accessory function for T cell proliferation in response to the superantigen TSST-1 and the mitogen Con A.