期刊
JOURNAL OF IMMUNOLOGY
卷 176, 期 7, 页码 4343-4351出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.176.7.4343
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- NCRR NIH HHS [C06 RR-12088] Funding Source: Medline
- NIAID NIH HHS [R01 AI051354-01, R01 AI051354-04, R01 AI051354, AI51354, R01 AI051354-03, R01 AI051354-05A2, R01 AI051354-02] Funding Source: Medline
Rapidly developing Ab responses to influenza virus provide immune protection even during a primary infection. How these early B cell responses are regulated is incompletely understood. In this study, we show that the first direct stimulatory signal for local respiratory tract B cells during influenza virus infection is provided through the type I IFNR. IFNR-mediated signals were responsible for the influenza infection-induced local but not systemic up-regulation of CD69 and CD86 on virtually all lymph node B cells and for induction of a family of IFN-regulated genes within 48 h of infection. These direct IFNR-mediated signals were shown to affect both the magnitude and quality of the local virus-specific Ab response. Thus, ligand(s) of the type I IFNR are direct nonredundant early innate signals that regulate local antiviral B cell responses.
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