NK-cells are involved in thymic atrophy induced   by influenza A virus infection.
NK-cells have traditionally been viewed as innate effector lymphocytes that serve as a first line of defence against a range of viruses and tumours. More recently, the importance of NK-cell immunoregulatory functions has been highlighted. NK-cells can inhibit antiviral T-cell responses, and also play an important role in controlling harmful T-cell activity in autoimmunity and transplantation settings. Moreover, immunopathological effects of NK-cells during infection have been reported. Nevertheless, the phenotype and function of NK-cells in the thymus during influenza virus infection is not understood. In the present study, we demonstrated that influenza A virus (IAV) infection in mice led to severe thymic atrophy caused by increased thymic T-cell apoptosis and suppressed proliferation. We found that NK-cells played a critical role in this phenotype. IFN-c production by NK-cells was a contributing factor for thymic atrophy during IAV infection. Taken together, our data indicate that NK-cells are involved in the thymic atrophy associated with IAV infection.
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, PR China.|Center for Influenza Research and Early-warning (CASCIRE), Chinese Academy of Sciences, Beijing, PR China.
Xuefeng
X
Duan
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, PR China.|Center for Influenza Research and Early-warning (CASCIRE), Chinese Academy of Sciences, Beijing, PR China.|University of Chinese Academy of Sciences, Beijing, PR China.
Jiao
J
Lu
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, PR China.|Center for Influenza Research and Early-warning (CASCIRE), Chinese Academy of Sciences, Beijing, PR China.
Kai
K
Zhou
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, PR China.|Center for Influenza Research and Early-warning (CASCIRE), Chinese Academy of Sciences, Beijing, PR China.|University of Chinese Academy of Sciences, Beijing, PR China.
Jing
J
Wang
Department of Pathology, 306 Hospital of PLA, Beijing, PR China.
Jihua
J
Wu
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, PR China.|Center for Influenza Research and Early-warning (CASCIRE), Chinese Academy of Sciences, Beijing, PR China.
George
G
Fu Gao
CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, PR China.|Center for Influenza Research and Early-warning (CASCIRE), Chinese Academy of Sciences, Beijing, PR China.
Min
M
Fang
D000818:Animals; D001284:Atrophy / Q000276:immunology / Q000821:virology; D005260:Female; D006801:Humans; D053118:Influenza A Virus, H1N1 Subtype / Q000502:physiology*; D007251:Influenza, Human / Q000276:immunology / Q000473:pathology / Q000821:virology*; D007371:Interferon-gamma / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D013950:Thymus Gland / Q000276:immunology* / Q000473:pathology
D007371:Interferon-gamma