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Mice transgenic for a soluble form of murine cytotoxic T lymphocyte antigen 4 are refractory to murine acquired immune deficiency sydrome development
Author(s) -
De Leval L.,
Debrus S.,
Lane P.,
Boniver J.,
Moutschen M.
Publication year - 1999
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.1365-2567.1999.00900.x
Subject(s) - cytotoxic t cell , biology , immune system , immunology , genetically modified mouse , transgene , cd28 , antigen , virology , t lymphocyte , t cell , gene , genetics , in vitro
Summary Interactions between B and CD4 + T cells are central to the pathogenesis of retrovirus‐induced murine acquired immune deficiency virus (MAIDS). Prompted by previous work showing that treatment with cytotoxic T lymphocyte antigen 4 immunoglobulin (CTLA4Ig) partly inhibited the disease, we studied the course of infection in mice deficient for CD28–B7 interactions (mCTLA4‐Hγ1 transgenic mice). Despite a relative viral load identical to that of non‐transgenic mice, the transgenic mice did not develop any of the major MAIDS symptoms (i.e. lymphoproliferation and immune anergy). The mCTLA4‐Hγ1 did not however, completely inhibit B‐cell activation as indicated by a slight hypergammaglobulinaemia and microscopic blastic transformation. Absence of MAIDS in transgenic mice was associated with much lower levels of both interleukin‐4 and interferon‐γ transcripts following viral infection. These results support the theory that the CD28/B7 costimulatory pathway is a critical determinant to MAIDS development.