期刊
JOURNAL OF IMMUNOLOGY
卷 189, 期 5, 页码 2521-2529出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1201125
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资金
- National Institute of Allergy and Infectious Diseases, National Institutes of Health
- U.K. Medical Research Council [U117581330]
- Medical Research Council [MC_U117581330] Funding Source: researchfish
- MRC [MC_U117581330] Funding Source: UKRI
The immune system is tasked with defending against a myriad of microbial infections, and its response to a given infectious microbe may be strongly influenced by coinfection with another microbe. It was shown that infection of mice with lactate dehydrogenase-elevating virus (LDV) impairs early adaptive immune responses to Friend virus (FV) coinfection. To investigate the mechanism of this impairment, we examined LDV-induced innate immune responses and found LDV-specific induction of IFN-alpha and IFN-gamma. LDV-induced IFN-alpha had little effect on FV infection or immune responses, but unexpectedly, LDV-induced IFN-gamma production dampened Th1 adaptive immune responses and enhanced FV infection. Two distinct effects were identified. First, LDV-induced IFN-gamma signaling indirectly modulated FV-specific CD8(+) T cell responses. Second, intrinsic IFN-gamma signaling in B cells promoted polyclonal B cell activation and enhanced early FV infection, despite promotion of germinal center formation and neutralizing Ab production. Results from this model reveal that IFN-gamma production can have detrimental effects on early adaptive immune responses and virus control. The Journal of Immunology, 2012, 189: 2521-2529.
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