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,,
Departments of
*
Pediatrics and
Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, Ontario, Canada;
Division of Virology and Molecular Immunology, Research Institute, Children’s Hospital of Eastern Ontario, Ottawa, Ontario, Canada;
Division of Infectious Diseases, Department of Medicine, Vancouver Hospital, University of British Columbia, Vancouver, British Columbia, Canada; and
¶ Health Canada, Therapeutic Products Program, Research Services Division, Ottawa, Ontario, Canada
The costimulatory molecule B7.2 (CD86) plays a vital role in immune
activation and development of Th responses. The molecular mechanisms by
which B7.2 expression is regulated are not understood. We investigated
the role of mitogen-activated protein kinases (MAPK) in the regulation
of B7.2 expression in LPS-stimulated human monocytic cells. LPS
stimulation of human monocytes resulted in the down-regulation of B7.2
expression that could be abrogated by anti-IL-10 Abs. Furthermore,
SB202190, a specific inhibitor of p38 MAPK, inhibited LPS-induced IL-10
production and reversed B7.2 down-regulation, suggesting that
LPS-induced B7.2 down-regulation may be mediated, at least in part, via
regulation of IL-10 production by p38 MAPK. In contrast to human
promonocytic THP-1 cells that are refractory to the inhibitory
effects of IL-10, LPS stimulation enhanced B7.2 expression. This
IL-10-independent B7.2 induction was not influenced by specific
inhibitors of either p38 or p42/44 MAPK. To ascertain the role of the
c-Jun N-terminal kinase (JNK) MAPK, dexamethasone, an inhibitor of JNK
activation, was used, which inhibited LPS-induced B7.2 expression.
Transfection of THP-1 cells with a plasmid expressing a
dominant-negative stress-activated protein/extracellular
signal-regulated kinase kinase 1 significantly reduced
LPS-induced B7.2 expression, thus confirming the involvement of JNK. To
study the signaling events downstream of JNK activation, we show that
dexamethasone did not inhibit LPS-induced NF-
B activation in THP-1
cells, suggesting that JNK may not be involved in NF-B activation
leading to B7.2 expression. Taken together, our results reveal the
distinct involvement of p38 in IL-10-dependent, and JNK in
IL-10-independent regulation of B7.2 expression in LPS-stimulated
monocytic cells.
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