tetano
Editor, Senior Moderator
J Virol. 2012 Jul 25. [Epub ahead of print]
TLR7 recognition is dispensable for influenza virus A infection, but important for the induction of hemagglutinin-specific antibodies in response to the 2009 pandemic split vaccine in mice.
Jeisy-Scott V, Kim JH, Davis WG, Cao W, Katz JM, Sambhara S.
Source
Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, GA 30333, USA.
Abstract
Recognition of pathogen associated molecular patterns by pattern recognition receptors of the innate immune system is crucial for the initiation of innate and adaptive responses and for immunological memory. We investigated the role of TLR7 in the induction of adaptive immunity and long-term memory following influenza virus infection and vaccination in C57Bl/6 mice. During infection with influenza A/PR8/34 virus, the absence of either TLR7 or MyD88 leads to reduced serum IgM and fewer IgM secreting B-cells in their secondary lymphoid organs, particularly in bone marrow. In spite of this, the absence of TLR7/MyD88 signaling did not impair the production of protective antibodies. Following immunization with the 2009 pandemic inactivated split vaccine, TLR7(-/-) mice had significantly lower levels of germinal center formation, antibody secreting cells and circulating influenza-specific antibodies than control animals. Consequently, TLR7(-/-) mice failed to develop protective immunological memory upon challenge. Furthermore, the immunogenicity of the split vaccine was likely due to TLR7 recognition of virion RNA, as its removal from the split vaccine significantly reduced the levels of influenza-specific antibodies, and compromised the vaccine protective efficacy in mice. Taken together, our data demonstrate that TLR7 plays an important role in vaccine-induced humoral immune responses to influenza through the interaction with viral RNA present in the split vaccine.
PMID:
22837197
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22837197
TLR7 recognition is dispensable for influenza virus A infection, but important for the induction of hemagglutinin-specific antibodies in response to the 2009 pandemic split vaccine in mice.
Jeisy-Scott V, Kim JH, Davis WG, Cao W, Katz JM, Sambhara S.
Source
Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, GA 30333, USA.
Abstract
Recognition of pathogen associated molecular patterns by pattern recognition receptors of the innate immune system is crucial for the initiation of innate and adaptive responses and for immunological memory. We investigated the role of TLR7 in the induction of adaptive immunity and long-term memory following influenza virus infection and vaccination in C57Bl/6 mice. During infection with influenza A/PR8/34 virus, the absence of either TLR7 or MyD88 leads to reduced serum IgM and fewer IgM secreting B-cells in their secondary lymphoid organs, particularly in bone marrow. In spite of this, the absence of TLR7/MyD88 signaling did not impair the production of protective antibodies. Following immunization with the 2009 pandemic inactivated split vaccine, TLR7(-/-) mice had significantly lower levels of germinal center formation, antibody secreting cells and circulating influenza-specific antibodies than control animals. Consequently, TLR7(-/-) mice failed to develop protective immunological memory upon challenge. Furthermore, the immunogenicity of the split vaccine was likely due to TLR7 recognition of virion RNA, as its removal from the split vaccine significantly reduced the levels of influenza-specific antibodies, and compromised the vaccine protective efficacy in mice. Taken together, our data demonstrate that TLR7 plays an important role in vaccine-induced humoral immune responses to influenza through the interaction with viral RNA present in the split vaccine.
PMID:
22837197
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22837197