Innate and adaptive immune responses to viral infection and vaccination

2011 ◽  
Vol 1 (4) ◽  
pp. 226-232 ◽  
Author(s):  
Taiki Aoshi ◽  
Shohei Koyama ◽  
Kouji Kobiyama ◽  
Shizuo Akira ◽  
Ken J Ishii
Cell Reports ◽  
2020 ◽  
Vol 31 (2) ◽  
pp. 107494 ◽  
Author(s):  
Lamin B. Cham ◽  
Laughing Bear Torrez Dulgeroff ◽  
Michal Caspi Tal ◽  
Tom Adomati ◽  
Fanghui Li ◽  
...  

Epilepsia ◽  
2010 ◽  
Vol 51 (3) ◽  
pp. 454-464 ◽  
Author(s):  
Nikki J. Kirkman ◽  
Jane E. Libbey ◽  
Karen S. Wilcox ◽  
H. Steve White ◽  
Robert S. Fujinami

2009 ◽  
Vol 206 (10) ◽  
pp. 2235-2251 ◽  
Author(s):  
Seung-Hwan Lee ◽  
Kwang-Sin Kim ◽  
Nassima Fodil-Cornu ◽  
Silvia M. Vidal ◽  
Christine A. Biron

Natural killer (NK) cells have the potential to deliver both direct antimicrobial effects and regulate adaptive immune responses, but NK cell yields have been reported to vary greatly during different viral infections. Activating receptors, including the Ly49H molecule recognizing mouse cytomegalovirus (MCMV), can stimulate NK cell expansion. To define Ly49H's role in supporting NK cell proliferation and maintenance under conditions of uncontrolled viral infection, experiments were performed in Ly49h−/−, perforin 1 (Prf1)−/−, and wild-type (wt) B6 mice. NK cell numbers were similar in uninfected mice, but relative to responses in MCMV-infected wt mice, NK cell yields declined in the absence of Ly49h and increased in the absence of Prf1, with high rates of proliferation and Ly49H expression on nearly all cells. The expansion was abolished in mice deficient for both Ly49h and Prf1 (Ly49h−/−Prf1−/−), and negative consequences for survival were revealed. The Ly49H-dependent protection mechanism delivered in the absence of Prf1 was a result of interleukin 10 production, by the sustained NK cells, to regulate the magnitude of CD8 T cell responses. Thus, the studies demonstrate a previously unappreciated critical role for activating receptors in keeping NK cells present during viral infection to regulate adaptive immune responses.


2021 ◽  
Vol 12 ◽  
Author(s):  
Baoxin Zhao ◽  
Weijie Wang ◽  
Yan Zhao ◽  
Hongxiu Qiao ◽  
Zhiyun Gao ◽  
...  

Host innate and adaptive immune responses play a vital role in clearing infected viruses. Meanwhile, viruses also evolve a series of mechanisms to weaken the host immune responses and evade immune defense. Recently, N6-methyladenosine (m6A), the most prevalent mRNA modification, has been revealed to regulate multiple steps of RNA metabolism, such as mRNA splicing, localization, stabilization, and translation, thus participating in many biological phenomena, including viral infection. In the process of virus–host interaction, the m6A modification that presents on the virus RNA impedes capture by the pattern recognition receptors, and the m6A modification appearing on the host immune-related molecules regulate interferon response, immune cell differentiation, inflammatory cytokine production, and other immune responses induced by viral infection. This review summarizes the research advances about the regulatory role of m6A modification in the innate and adaptive immune responses during viral infections.


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