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  3. Clonal Vγ6+Vδ4+ T cells promote IL-17-mediated immunity against Staphylococcus aureus skin infection

Clonal Vγ6+Vδ4+ T cells promote IL-17-mediated immunity against Staphylococcus aureus skin infection

  • Proc Natl Acad Sci U S A. 2019 May 28;116(22):10917-10926. doi: 10.1073/pnas.1818256116.
Mark C Marchitto 1,  Carly A Dillen 1,  Haiyun Liu 1,  Robert J Miller 1,  Nathan K Archer 1,  Roger V Ortines 1,  Martin P Alphonse 1,  Alina I Marusina 2,  Alexander A Merleev 2,  Yu Wang 1,  Bret L Pinsker 1,  Angel S Byrd 1,  Isabelle D Brown 1,  Advaitaa Ravipati 1,  Emily Zhang 1,  Shuting S Cai 1,  Nathachit Limjunyawong 3 4,  Xinzhong Dong 3 4 5,  Michael R Yeaman 6 7 8 9,  Scott I Simon 10,  Wei Shen 11,  Scott K Durum 11,  Rebecca L O'Brien 12 13,  Emanual Maverakis 2,  Lloyd S Miller 14 15 16 17
Affiliations

Affiliations

  • 1 Department of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD 21231.
  • 2 Department of Dermatology, School of Medicine, University of California, Davis, Sacramento, CA 95817.
  • 3 The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
  • 4 The Center for Sensory Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
  • 5 Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
  • 6 Division of Molecular Medicine, Harbor-UCLA Medical Center, Torrance, CA 90502.
  • 7 Division of Infectious Diseases, Harbor-UCLA Medical Center, Torrance, CA 90502.
  • 8 Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095.
  • 9 Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, Torrance, CA 90502.
  • 10 Department of Biomedical Engineering, University of California, Davis, CA 95616.
  • 11 Cytokines and Immunity Section, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
  • 12 Department of Biomedical Research, National Jewish Health, Denver, CO 80206.
  • 13 Department of Immunology and Microbiology, University of Colorado Health Sciences Center, Aurora, CO 80206.
  • 14 Department of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD 21231; lloydmiller@jhmi.edu.
  • 15 Department of Medicine, Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD 21287.
  • 16 Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287.
  • 17 Department of Materials Science and Engineering, Johns Hopkins University, Baltimore, MD 21218.
PMID: 31088972 DOI: 10.1073/pnas.1818256116
Abstract

T cell cytokines contribute to immunity against Staphylococcus aureus, but the predominant T cell subsets involved are unclear. In an S. aureus skin Infection mouse model, we found that the IL-17 response was mediated by γδ T cells, which trafficked from lymph nodes to the infected skin to induce neutrophil recruitment, proinflammatory cytokines IL-1α, IL-1β, and TNF, and host defense peptides. RNA-seq for TRG and TRD sequences in lymph nodes and skin revealed a single clonotypic expansion of the encoded complementarity-determining region 3 amino acid sequence, which could be generated by canonical nucleotide sequences of TRGV5 or TRGV6 and TRDV4 However, only TRGV6 and TRDV4 but not TRGV5 sequences expanded. Finally, Vγ6+ T cells were a predominant γδ T cell subset that produced IL-17A as well as IL-22, TNF, and IFNγ, indicating a broad and substantial role for clonal Vγ6+Vδ4+ T cells in immunity against S. aureus skin infections.

Keywords

IL-17; Staphylococcus aureus; T cells; neutrophils; skin.

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