tetano
Editor, Senior Moderator
Vaccine. 2012 Oct 22. pii: S0264-410X(12)01485-5. doi: 10.1016/j.vaccine.2012.10.039. [Epub ahead of print]
Trivalent inactivated influenza vaccines induce broad immunological reactivity to both internal virion components and influenza surface proteins.
Richards KA, Chaves FA, Alam S, Sant AJ.
Source
David H. Smith Center for Vaccine Biology and Immunology, Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, United States.
Abstract
There are a number of related goals of influenza vaccination, including elicitation of protective antibodies and induction of cellular CD4 and CD8T cell responses. Because CD4T cell expansion and functionality are influenced by peptide specificity and T cell gene expression can be modified by repeated re-stimulations, it is important to evaluate how frequent influenza vaccinations affect CD4T cell dependent functions in protective immunity to influenza. Trivalent influenza vaccines (TIV) have production of neutralizing antibodies to HA as their primary goal and main criteria for efficacy. Accordingly, they are not characterized for any other viral components. In the current study, we evaluated whether other influenza virus proteins were present in commercial TIV at levels sufficient for immunogenicity in vivo. Mice that differed with regard to their expressed class II molecules were used in concert with peptide-stimulated cytokine ELISPOT assays to comprehensively evaluate the CD4T cell antigen specificity induced by the TIV. Our studies revealed that NA, NP, M1 and NS1 were present in sufficient quantities in the TIV to prime and boost CD4T cells. These results suggest that in humans, the broad CD4T cell repertoire induced by live infection is continually boosted and maintained throughout life by regular vaccination with licensed intramuscular split vaccines. The implications raised by our findings on CD4T cell functionality in influenza are discussed.
Copyright ? 2012. Published by Elsevier Ltd.
PMID:
23099328
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23099328
Trivalent inactivated influenza vaccines induce broad immunological reactivity to both internal virion components and influenza surface proteins.
Richards KA, Chaves FA, Alam S, Sant AJ.
Source
David H. Smith Center for Vaccine Biology and Immunology, Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, United States.
Abstract
There are a number of related goals of influenza vaccination, including elicitation of protective antibodies and induction of cellular CD4 and CD8T cell responses. Because CD4T cell expansion and functionality are influenced by peptide specificity and T cell gene expression can be modified by repeated re-stimulations, it is important to evaluate how frequent influenza vaccinations affect CD4T cell dependent functions in protective immunity to influenza. Trivalent influenza vaccines (TIV) have production of neutralizing antibodies to HA as their primary goal and main criteria for efficacy. Accordingly, they are not characterized for any other viral components. In the current study, we evaluated whether other influenza virus proteins were present in commercial TIV at levels sufficient for immunogenicity in vivo. Mice that differed with regard to their expressed class II molecules were used in concert with peptide-stimulated cytokine ELISPOT assays to comprehensively evaluate the CD4T cell antigen specificity induced by the TIV. Our studies revealed that NA, NP, M1 and NS1 were present in sufficient quantities in the TIV to prime and boost CD4T cells. These results suggest that in humans, the broad CD4T cell repertoire induced by live infection is continually boosted and maintained throughout life by regular vaccination with licensed intramuscular split vaccines. The implications raised by our findings on CD4T cell functionality in influenza are discussed.
Copyright ? 2012. Published by Elsevier Ltd.
PMID:
23099328
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23099328