|dc.contributor.author||Sung Su Yea||-|
|dc.description.abstract||This study examined the immunomodulatory effects of hydrogen peroxide (H2O2) in B6C3F1 mouse splenic lymphocytes. H2O2 produced a marked and dose-related inhibition of both lipopolysaccharide (LPS)-induced B-cell proliferation and concanavalin A (Con A)-induced T-cell proliferation. Unexpectedly, little effect was observed with H2O2 on the antibody-forming cell (AFC) response to the polyclonal B-cell activator, LPS. It was also observed that H2O2 did not have any detectable effect on forskolin-stimulated adenylate cyclase, indicating that cyclic AMP (cAMP) is not a mediator of H2O2-induced suppression of the immune response. Rather, LPS-induced activation of protein kinase C (PKC) was completely inhibited when cells were pretreated with H2O2 for 18 h, although PKC activity was increased approximately twofold following treatment with H2O2 for 10 min. In addition, H2O2 pretreatment blocked the phosphorylation of two stress-activated mitogen-activated protein kinases (MAPKs), c-Jun N-terminal kinase (JNK) and p38 by LPS in a concentration-dependent fashion. Therefore, these data suggest that H2O2 suppresses immune response through the desensitization of PKC, which subsequently results in inhibition of JNK and p38.||-|
|dc.title||Hydrogen peroxide inhibits the immune response to lipopolysaccharide by attenuating signaling through c-Jun N-terminal kinase and p38 associated with protein kinase C||-|
|dc.title.alternative||Hydrogen peroxide inhibits the immune response to lipopolysaccharide by attenuating signaling through c-Jun N-terminal kinase and p38 associated with protein kinase C||-|
|dc.identifier.bibliographicCitation||Immunopharmacology, vol. 48, no. 2, pp. 165-172||-|
|dc.subject.keyword||protein kinase C||-|
|dc.subject.local||Protein kinase C||-|
|dc.subject.local||protein kinase C||-|
|dc.subject.local||protein kinase c||-|
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