Abstract:
:Galectin-9 is a pleiotropic immune modulator affecting numerous cell types of innate and adaptive immunity. Patients with chronic infection with either hepatitis C virus (HCV) or HIV have elevated circulating levels. Limited data exist on the regulation of natural killer (NK) cell function through interaction with galectin-9. We found that galectin-9 ligation downregulates multiple immune-activating genes, including eight involved in the NK cell-mediated cytotoxicity pathway, impairs lymphokine-activated killing, and decreases the proportion of gamma interferon (IFN-γ)-producing NK cells that had been stimulated with interleukin-12 (IL-12)/IL-15. We demonstrate that the transcriptional and functional changes induced by galectin-9 are independent of Tim-3. Consistent with these results for humans, we find that the genetic absence of galectin-9 in mice is associated with greater IFN-γ production by NK cells and enhanced degranulation. We also show that in the setting of a short-term (4-day) murine cytomegalovirus infection, terminally differentiated NKs accumulate in the livers of galectin-9 knockout mice, and that hepatic NKs spontaneously produce significantly more IFN-γ in this setting. Taken together, our results indicate that galectin-9 engagement impairs the function of NK cells, including cytotoxicity and cytokine production.
journal_name
J Viroljournal_title
Journal of virologyauthors
Golden-Mason L,McMahan RH,Strong M,Reisdorph R,Mahaffey S,Palmer BE,Cheng L,Kulesza C,Hirashima M,Niki T,Rosen HRdoi
10.1128/JVI.01085-12subject
Has Abstractpub_date
2013-05-01 00:00:00pages
4835-45issue
9eissn
0022-538Xissn
1098-5514pii
JVI.01085-12journal_volume
87pub_type
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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