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Oncogene Transformation can induce Tolerogenicity in Murine Macrophages after Down‐Regulation of Immunogenicity without altering Major Histocompatibility Complex Antigen Expression
Author(s) -
WOTTGE H.U.,
ECKSTEIN V.,
SELIGER B.,
MÜLLERRUCHHOLTZ W.
Publication year - 1993
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1993.tb01693.x
Subject(s) - biology , immunogenicity , clone (java method) , major histocompatibility complex , antigen , microbiology and biotechnology , cytotoxic t cell , t cell , immunology , immune system , in vitro , gene , genetics
In vitro studies on cell lines may allow analyses of the mechanisms of immunogenicity and tolerogenicity in cells. We used a model of oncogenic transformation of an established murine macrophage cell line and report here that one v‐mos‐transformed clone expressing unaltered high amounts of MHC class I and II antigens does not induce proliferation of unprimed T cells in primary mixed lymphocyte reactions, in sharp contrast to its non‐transformed parental cells. Interestingly, this clone induces specific unrespon‐siveness, as revealed by the lack of responsiveness of MHC‐specific T cells when subsequently exposed to the pertinent MHC alloantigens in immunogenic form but unaltered MHC‐third party responsiveness of the naive spleen T cells. Furthermore, the accessory function of this clone is strongly reduced. These functional defects could be overcome by the addition of exogenous interleukin‐1α (IL‐1α). Analysis of mRNA expression showed a significant and selective reduction of IL‐1α mRNA levels when compared with parental cells.