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‘Ignorance’ of Antigen‐Specific Murine CD4 + and CD8 + T Cells is Overruled by Lipopolysaccharide and Leads to Specific Induction of IFN‐γ *
Author(s) -
Moré S. H.,
Breloer M.,
Fentz A.K.,
Fleischer B.,
Von Bonin A.
Publication year - 2002
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 - 10.1046/j.1365-3083.2002.01061.x
Subject(s) - biology , natural killer t cell , cytotoxic t cell , antigen , major histocompatibility complex , t cell , antigen presenting cell , interleukin 21 , microbiology and biotechnology , il 2 receptor , cd8 , interleukin 12 , immunology , immune system , in vitro , biochemistry
Lipopolysaccharide (LPS) can activate human and murine T cells in vivo and in vitro . Here we analysed the effects of LPS on T cells with defined specificities in T‐cell receptor (TCR)‐transgenic systems. LPS rapidly induced high amounts of interferon (IFN)‐γ in a subpopulation of purified T cells from DO11.10 (OVA 323–339 /H2‐A d ) and OT‐1 (OVA 257–264 /H2‐K b ) mice when coincubated with antigen‐pulsed peritoneal exudate cells (PECs). LPS induced IFN‐γ in T cell cultures even when the number of antigenic major histocompatibility complex (MHC) class‐I complexes was too small to stimulate the T cells. LPS, thus, overruled the unresponsiveness of the otherwise ‘antigen‐ignorant’ T cells. The release of IFN‐γ strictly correlates with the PECs' ability to produce interleukin (IL)‐12. In contrast to the induction of IFN‐γ, antigen‐specific IL‐2 secretion and proliferation of T cells were rather decreased in the presence of LPS. Only very few IFN‐γ‐secreting natural killer (NK) cells and natural killer T (NKT) cells in the given experimental system could be detected using intracellular fluorescence‐activated cell sorter (FACS) staining. Taken together, our results indicate that LPS has the potential to activate quiescent T cells and to specifically induce IFN‐γ in CD4 and CD8 T cells. This may have direct consequences for the activation of autoreactive T cells following bacterial infections.