@article{47aec900c0604432b774b36e1c47f8ba,
title = "KIR+CD8+ T cells suppress pathogenic T cells and ar active in autoimmune diseases and COVID-19",
abstract = "In this work, we find that CD8+ T cells expressing inhibitory killer cell immunoglobulin-like receptors (KIRs) are the human equivalent of Ly49+CD8+ regulatory T cells in mice and are increased in the blood and inflamed tissues of patients with a variety of autoimmune diseases. Moreover, these CD8+ T cells efficiently eliminated pathogenic gliadin-specific CD4+ T cells from the leukocytes of celiac disease patients in vitro. We also find elevated levels of KIR+CD8+ T cells, but not CD4+ regulatory T cells, in COVID-19 patients, correlating with disease severity and vasculitis. Selective ablation of Ly49+CD8+ T cells in virus-infected mice led to autoimmunity after infection. Our results indicate that in both species, these regulatory CD8+ T cells act specifically to suppress pathogenic T cells in autoimmune and infectious diseases.",
author = "Jing Li and Maxim Zaslavsky and Yapeng Su and Jing Guo and Sikora, {Michael J.} and {van Unen}, Vincent and Asbj{\o}rn Christophersen and Chiou, {Shin Heng} and Liang Chen and Jiefu Li and Xuhuai Ji and Julie Wilhelmy and McSween, {Alana M.} and Palanski, {Brad A.} and Mallajosyula, {Venkata Vamsee Aditya} and Bracey, {Nathan A.} and Dhondalay, {Gopal Krishna R.} and Kartik Bhamidipati and Joy Pai and Kipp, {Lucas B.} and Dunn, {Jeffrey E.} and Hauser, {Stephen L.} and Oksenberg, {Jorge R.} and Satpathy, {Ansuman T.} and Robinson, {William H.} and Dekker, {Cornelia L.} and Steinmetz, {Lars M.} and Chaitan Khosla and Utz, {Paul J.} and Sollid, {Ludvig M.} and Chien, {Yueh Hsiu} and Heath, {James R.} and Fernandez-Becker, {Nielsen Q.} and Nadeau, {Kari C.} and Naresha Saligrama and Davis, {Mark M.}",
note = "Funding Information: We are grateful for funding by the National Institute of Allergy and Infectious Diseases (NIAID) (U19-AI057229) and the Howard Hughes Medical Institute to M.M.D. The collection of MS samples was supported by a grant from the National Multiple Sclerosis Society (NMSS), RG-1611-26299. This work was partially supported by pilot funding from the Stanford Diabetes Research Center (P30DK116074). The project described was also supported in part by award no. 1S10OD010580-01A1 from the National Center for Research Resources (NCRR). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NCRR or the National Institutes of Health (NIH). M.Z. was supported by a National Science Foundation Graduate Research Fellowship. J.R.H. and Y.S. were funded by the Wilke Family Foundation, Merck, and the Biomedical Advanced Research and Development Authority under contract no. HHSO10201600031C. L.M.St. and M.J.S. were supported by NIAID under award no. R01AI139550. S.L.H. is supported by the NIH/NINDS (R35NS111644) and the Valhalla Foundation. C.L.D. received funding from NIAID under award nos. U19-AI057229 and U19-AI090019. C.K. was funded by NIH R01DK063158. P.J.U. was supported by NIAID (R01AI125197-04) and the Henry Gustav Floren Trust. K.C.N. was funded by the Sunshine Foundation and the Sean N. Parker Center at Stanford University. N.S. was supported by a postdoctoral fellowship and a Career Transition grant from NMSS. Author Publisher Copyright: Copyright {\textcopyright} 2022 The Authors.",
year = "2022",
month = apr,
day = "15",
doi = "10.1126/science.abi9591",
language = "English",
volume = "376",
journal = "Science",
issn = "0036-8075",
number = "6590",
}