CXCL9 compensates for the absence of CXCL10 during recurrent Herpetic stromal keratitis.
CXCL9 compensates for the absence of CXCL10 during recurrent Herpetic stromal keratitis.
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DOI：
10.1016/j.virol.2017.02.022
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发表时间：
2017-06
期刊：
影响因子：
3.7
通讯作者：
Stuart PM
中科院分区：
文献类型：
--
作者：
Tajfirouz D;West DM;Yin XT;Potter CA;Klein R;Stuart PM
Herpetic stromal keratitis (HSK) is a disease that is typically associated with reactivation of a latent HSV-1 infection. This disease is driven, in part, by chemokines that recruit leukocytes to the cornea. Surprisingly, neutralization of CXCL10 significantly reduced disease, while B6-CXCL10−/− mice exhibited worse disease compared with similarly infected wild-type controls. We hypothesized that compensatory up-regulation of CXCL9 occurs in the absence of CXCL10. Analysis of CXCL9 expression in HSV-1-infected B6 mice and B6-CXCL10−/− mice revealed significantly more CXCL9 in B6-XCL10−/− mice. Treatment of B6 and B6-CXCL10−/− mice with neutralizing antibodies to CXCL9 reduced HSK scores in B6-CXCL10−/−, but not B6 mice. We conclude that CXCL10 production worsens HSK and that CXCL9 may compensate in CXCL10-deficient animals. These studies identify the critical role that CXCL10 plays in the pathogenesis of recurrent HSK, and that CXCL9 displays its importance when CXCL10 is absent.
