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Lipopolysaccharide‐dependent down‐regulation of CD27 expression on T cells activated with superantigen
Author(s) -
Kenzo Kai,
Hidemi Rikiishi,
Shunji Sugawara,
Masae Takahashi,
Haruhiko Takada,
Katsuo Kumagai
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.1365-2567.1999.00857.x
Subject(s) - superantigen , lipopolysaccharide , microbiology and biotechnology , expression (computer science) , chemistry , immunology , biology , t cell , computer science , immune system , programming language
To investigate the mechanisms underlying T‐cell responses during superantigen (SAg) stimulation, we analysed the effects of SAg on CD27 expression with or without lipopolysaccharide (LPS) as a novel regulator of T‐cell function. CD27 is expressed on the majority of resting peripheral blood T cells (CD27 low ). Activation of T cells by SAg induces high levels of CD27 surface expression (CD27 high ) accompanied with simultaneous CD30 receptor expression. After prolonged activation in vitro , the level of CD27 expression became intermediate. The effects of LPS on down‐regulation of CD27 high expression on CD30 + T cells were dose‐dependent. Separating LPS‐stimulated monocytes from T cells by mechanical dispersion abolished its inhibitory effect, indicating the requirement for direct interactions between monocytes and T cells. We also found that SAg up‐regulated CD80 expression on CD14 + monocytes and LPS inhibited SAg‐induced CD80 expression after 24 hr of stimulation. Up‐regulation of CD152 (CTLA‐4) was selective, since it was found to be preferentially expressed on the CD30 + population. Competitive experiments using soluble blocking peptides showed that addition of CD28 or CD80 peptide recovered LPS‐induced down‐regulation of CD27 high expression on CD30 + T cells. These observations suggested that the presence of low levels of CD80 on monocytes may partially inhibit CD27 expression due to inefficient delivery of positive signals via CD28/CD80 interaction, and that the increased levels of CD80 enhance the inhibition through interactions with CD152 which is expressed at the highest levels after 48 hr of activation.