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J Infect Dis. 2016 Jul 15;214(2):248-57. doi: 10.1093/infdis/jiw126. Epub 2016 Mar 30.

Autoimmune Variant PTPN22 C1858T Is Associated With Impaired Responses to Influenza Vaccination.

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Center for Immunology Division of Rheumatic and Autoimmune Diseases, Department of Medicine, University of Minnesota Medical School.
Department of Microbiology, School of Graduate Studies, Icahn School of Medicine at Mount Sinai, New York, New York.
Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis.
Center for Immunology.
Department of Biochemistry and Biomedical Sciences, Institute for Infectious Diseases Research, McMaster Immunology Research Center, McMaster University, Hamilton, Canada.


High-affinity-antibody production, T-cell activation, and interferon upregulation all contribute to protective immunity that occurs in humans following influenza immunization. Hematopoietic cell-specific PTPN22 encodes lymphoid phosphatase (Lyp), which regulates lymphocyte antigen receptor and pattern recognition receptor (PRR) signaling. A PTPN22 variant, R620W (LypW), predisposes to autoimmune and infectious diseases and confers altered signaling through antigen receptors and PRRs. We tested the hypothesis that LypW-bearing humans would have diminished immune response to trivalent influenza vaccine (TIV). LypW carriers exhibited decreased induction of influenza virus-specific CD4(+) T cells expressing effector cytokines and failed to increase antibody affinity following TIV receipt. No differences between LypW carriers and noncarriers were observed in virus-specific CD8(+) T-cell responses, early interferon transcriptional responses, or myeloid antigen-presenting cell costimulatory molecule upregulation. The association of LypW with defects in TIV-induced CD4(+) T-cell expansion and antibody affinity maturation suggests that LypW may predispose individuals to have a diminished capacity to generate protective immunity against influenza virus.


CD4 T cells; PTPN22; affinity; influenza; vaccine

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