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T cell‐ and perforin‐dependent depletion of B cells in vivo by staphylococcal enterotoxin A
Author(s) -
Anette Sundstedt,
Susanna Grundström,
Mikael Dohlsten
Publication year - 1998
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1998.00562.x
Subject(s) - enterotoxin , perforin , in vivo , microbiology and biotechnology , biology , immunology , chemistry , in vitro , cytotoxic t cell , escherichia coli , genetics , gene
Bacterial superantigens bind to major histocompatibility complex (MHC) class II and subsequently activate both CD4 + and CD8 + T lymphocytes expressing certain T‐cell receptor (TCR)‐Vβ chains. In response to superantigen exposure these subsets proliferate, produce large amounts of proinflammatory cytokines and in addition CD8 + cytotoxic T lymphocytes (CTL) are induced. Previous studies in vitro have shown that these CTL effectively lyse MHC class II‐expressing cells presenting the proper superantigen. However, it is unknown whether superantigens induce a similar response towards MHC class II + antigen‐presenting cells in vivo . In this study we demonstrate that administration of repeated injections of the superantigen staphylococcal enterotoxin A (SEA) to TCR‐Vβ3 transgenic mice results in a loss of MHC class II‐expressing cells in the spleen. Analysis of different MHC class II + subsets revealed a selective depletion of CD19 + B cells, while F4/80 + macrophages increased in number. Depletion of T cells with anti‐CD4 or anti‐CD8 monoclonal antibody indicated that CD8 + T cells were crucial for SEA‐induced cytotoxicity in vivo . Repeated injections of SEA to perforin‐deficient mice resulted in significantly less B‐cell depletion compared with control mice. This suggests that superantigen‐activated CD8 + T cells lyse MHC class II + antigen‐presenting cells in a perforin‐dependent manner in vivo . It is suggested that this represents a novel bacterial immune escape mechanism, which may particularly impair local humoral immune responses.