Human KIR + CD8 + T cells target pathogenic T cells in Celiac disease and are active in autoimmune diseases and COVID-19

Previous reports show that Ly49 + CD8 + T cells can suppress autoimmunity in mouse models of autoimmune diseases. Here we find a markedly increased frequency of CD8 + T cells expressing inhibitory Killer cell Immunoglobulin like Receptors (KIR), the human equivalent of the Ly49 family, in the blood and inflamed tissues of various autoimmune diseases. Moreover, KIR + CD8 + T cells can efficiently eliminate pathogenic gliadin-specific CD4 + T cells from Celiac disease (CeD) patients' leukocytes in vitro . Furthermore, we observe elevated levels of KIR + CD8 + T cells, but not CD4 + regulatory T cells, in COVID-19 and influenza-infected patients, and this correlates with disease severity and vasculitis in COVID-19. Expanded KIR + CD8 + T cells from these different diseases display shared phenotypes and similar T cell receptor sequences. These results characterize a regulatory CD8 + T cell subset in humans, broadly active in both autoimmune and infectious diseases, which we hypothesize functions to control self-reactive or otherwise pathogenic T cells.

ONE-SENTENCE SUMMARY: Here we identified KIR + CD8 + T cells as a regulatory CD8 + T cell subset in humans that suppresses self-reactive or otherwise pathogenic CD4 + T cells.

Errataetall:

UpdateIn: Science. 2022 Mar 8;:eabi9591. - PMID 35258337

Medienart:

E-Artikel

Erscheinungsjahr:

2021

Erschienen:

2021

Enthalten in:

Zur Gesamtaufnahme - year:2021

Enthalten in:

bioRxiv : the preprint server for biology - (2021) vom: 25. Dez.

Sprache:

Englisch

Beteiligte Personen:

Li, Jing [VerfasserIn]
Zaslavsky, Maxim [VerfasserIn]
Su, Yapeng [VerfasserIn]
Sikora, Michael J [VerfasserIn]
van Unen, Vincent [VerfasserIn]
Christophersen, Asbjørn [VerfasserIn]
Chiou, Shin-Heng [VerfasserIn]
Chen, Liang [VerfasserIn]
Li, Jiefu [VerfasserIn]
Ji, Xuhuai [VerfasserIn]
Wilhelmy, Julie [VerfasserIn]
McSween, Alana M [VerfasserIn]
Palanski, Brad A [VerfasserIn]
Aditya Mallajosyula, Venkata Vamsee [VerfasserIn]
Dhondalay, Gopal Krishna R [VerfasserIn]
Bhamidipati, Kartik [VerfasserIn]
Pai, Joy [VerfasserIn]
Kipp, Lucas B [VerfasserIn]
Dunn, Jeffrey E [VerfasserIn]
Hauser, Stephen L [VerfasserIn]
Oksenberg, Jorge R [VerfasserIn]
Satpathy, Ansuman T [VerfasserIn]
Robinson, William H [VerfasserIn]
Steinmetz, Lars M [VerfasserIn]
Khosla, Chaitan [VerfasserIn]
Utz, Paul J [VerfasserIn]
Sollid, Ludvig M [VerfasserIn]
Heath, James R [VerfasserIn]
Fernandez-Becker, Nielsen Q [VerfasserIn]
Nadeau, Kari C [VerfasserIn]
Saligrama, Naresha [VerfasserIn]
Davis, Mark M [VerfasserIn]

Links:

Volltext

Themen:

Preprint

Anmerkungen:

Date Revised 29.04.2022

published: Electronic

UpdateIn: Science. 2022 Mar 8;:eabi9591. - PMID 35258337

Citation Status PubMed-not-MEDLINE

doi:

10.1101/2021.12.23.473930

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM335165087