Helper T cell-dependent human B cell differentiation mediated by a mycoplasmal superantigen bridge. Academic Article uri icon

Overview

abstract

  • Experimentally induced murine graft-vs.-host disease may be characterized by hypergammaglobulinemia, autoantibody formation, and immune complex-mediated organ system damage that mimics SLE. These autoimmune phenomena are mediated by abnormal Th-B cell cooperation, across MHC disparities, in which donor-derived allospecific Th cells recognize and interact with MHC class II antigens on the surface of recipient B cells. Microbial toxins, termed superantigens, which bind to MHC class II molecules and activate selected T cells based on TCR variable gene usage, may induce a similar form of Th-B cell interaction. In the present study, we generated and characterized human Th cell lines reactive with the Mycoplasma arthritidis superantigen (MAM). The essential observation is that resting human B cells bind MAM and present it to superantigen-reactive autologous or allogeneic Th cells, resulting in both Th cell activation and a consequent polyclonal Ig response by the superantigen-bearing B cells.

publication date

  • June 1, 1990

Research

keywords

  • Antigens, Bacterial
  • B-Lymphocytes
  • Lymphocyte Activation
  • Mitogens
  • T-Lymphocytes, Helper-Inducer

Identity

PubMed Central ID

  • PMC2187950

Scopus Document Identifier

  • 0025293058

Digital Object Identifier (DOI)

  • 10.1084/jem.171.6.2153

PubMed ID

  • 2141059

Additional Document Info

volume

  • 171

issue

  • 6