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MHC class II‐independent CD25 + CD4 + CD8α β + α β T cells attenuate CD4 + T cell‐induced transfer colitis
Author(s) -
Krajina Tamara,
Leithäuser Frank,
Reimann Jörg
Publication year - 2004
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.200324463
Subject(s) - il 2 receptor , biology , microbiology and biotechnology , cytotoxic t cell , interleukin 21 , t cell , adoptive cell transfer , cd8 , antigen presenting cell , population , immunology , antigen , immune system , biochemistry , medicine , in vitro , environmental health
Abstract CD4 + α β T cell populations that develop in mice deficient in MHC class II (through ‘knockout’ of either the Aα, or the Aβ chain of the I‐A b molecule) comprise a major ‘single‐positive’ (SP) CD4 + CD8 – subset (60–90%) and a minor ‘double‐positive’ (DP) CD4 + CD8α β + subset (10–40%). Many DP T cells found in spleen, mesenteric lymph nodes (MLN) and colonic lamina propria (cLP) express CD25, CD103 and Foxp3. Adoptive transfer of SP but not DP T cells from Aα –/– or Aβ –/– B6 mice into congenic RAG –/– hosts induces colitis. Transfer of SP T cells repopulates the host with only SP T cells; transfer of DP T cells repopulates the host with DP and SP T cells. Anti‐CD25 antibody treatment of mice transplanted with DP T cells induces severe, lethal colitis; anti‐CD25 antibody treatment of mice transplanted with SP T cells further aggravates the course of severe colitis. Hence, regulatory CD25 + T cells within (or developing from) the DP T cell population of MHC class II‐deficient mice control the colitogenic potential of CD25 – CD4 + T cells.