| Literature DB >> 31088972 |
Mark C Marchitto1, Carly A Dillen1, Haiyun Liu1, Robert J Miller1, Nathan K Archer1, Roger V Ortines1, Martin P Alphonse1, Alina I Marusina2, Alexander A Merleev2, Yu Wang1, Bret L Pinsker1, Angel S Byrd1, Isabelle D Brown1, Advaitaa Ravipati1, Emily Zhang1, Shuting S Cai1, Nathachit Limjunyawong3,4, Xinzhong Dong3,4,5, Michael R Yeaman6,7,8,9, Scott I Simon10, Wei Shen11, Scott K Durum11, Rebecca L O'Brien12,13, Emanual Maverakis2, Lloyd S Miller14,15,16,17.
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.Entities:
Keywords: IL-17; Staphylococcus aureus; T cells; neutrophils; skin
Year: 2019 PMID： 31088972 PMCID： PMC6561199 DOI： 10.1073/pnas.1818256116
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205