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Therapeutic effect of IL-12/23 and their signaling pathway blockade on brain ischemia model.

Abstract：

:Recently, T cell cytokines such as IL-17 and IFN-γ have been shown to play important roles in the progression of brain injury induced by ischemia. We have shown that IL-23 from infiltrated macrophages activates γδT cells, thereby inducing IL-17 from these cells. However, deletion of the IL-23 gene in mice showed a more dramatic protective effect against brain ischemia reperfusion (I/R) model than γδT cell depletion did, suggesting that IL-23 plays some other pivotal role in brain injury in addition to its role in IL-17 induction. To develop therapeutic methods based on these findings, we examined the effect of the JAK kinase inhibitor CP-690550 and an anti-IL12/23 monoclonal antibody on an I/R model. CP-690550 efficiently inhibited IL-17 production from memory T cells in vitro and partly suppressed infarct volume increase after I/R. Anti-p40 antibody, which blocks both IL-12 and IL-23, efficiently suppressed I/R injury and improved recovery of neurological deficits. The number of IL-17-producing cells was decreased by anti-p40 antibody treatment. Thus the JAK inhibitor and anti-p40 antibody, both of which have already been under trial for the treatment of several human inflammatory diseases, appear to be promising therapeutic agents for the amelioration of stroke.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Konoeda F,Shichita T,Yoshida H,Sugiyama Y,Muto G,Hasegawa E,Morita R,Suzuki N,Yoshimura A

doi

10.1016/j.bbrc.2010.10.058

subject

Has Abstract

pub_date

2010-11-19 00:00:00

pages

500-6

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(10)01936-4

journal_volume

402

pub_type

杂志文章

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