• FluTrackers.com Inc. does not provide medical advice. Information on this web site is collected from various internet resources, and the FluTrackers board of directors makes no warranty to the safety, efficacy, correctness or completeness of the information posted on this site by any author or poster. The information collated here is for instructional and/or discussion purposes only and is NOT intended to diagnose or treat any disease, illness, or other medical condition. Every individual reader or poster should seek advice from their personal physician/healthcare practitioner before considering or using any interventions that are discussed on this website. By continuing to access this website you agree to consult your personal physican before using any interventions posted on this website, and you agree to hold harmless FluTrackers.com Inc., the board of directors, the members, and all authors and posters for any effects from use of any medication, supplement, vitamin or other substance, device, intervention, etc. mentioned in posts on this website, or other internet venues referenced in posts on this website.
  • We are not asking for any donations. Do not donate to any entity who says they are raising funds for us.

Sci Adv . PD-1/PD-L1 blockade abrogates a dysfunctional innate-adaptive immune axis in critical β-coronavirus disease

tetano

Editor, Senior Moderator
Sci Adv


. 2022 Sep 23;8(38):eabn6545.
doi: 10.1126/sciadv.abn6545. Epub 2022 Sep 21.
PD-1/PD-L1 blockade abrogates a dysfunctional innate-adaptive immune axis in critical β-coronavirus disease


Maite Duhalde Vega[SUP] 1 [/SUP], Daniela Olivera[SUP] 1 2 [/SUP], Gustavo Gastão Davanzo[SUP] 3 [/SUP], Mauricio Bertullo[SUP] 4 [/SUP], Verónica Noya[SUP] 5 [/SUP], Gabriela Fabiano de Souza[SUP] 6 [/SUP], Stéfanie Primon Muraro[SUP] 6 [/SUP], Icaro Castro[SUP] 7 [/SUP], Ana Paula Arévalo[SUP] 8 [/SUP], Martina Crispo[SUP] 8 [/SUP], Germán Galliussi[SUP] 9 [/SUP], Sofía Russo[SUP] 1 2 [/SUP], David Charbonnier[SUP] 1 [/SUP], Florencia Rammauro[SUP] 2 10 [/SUP], Mathías Jeldres[SUP] 1 2 [/SUP], Catalina Alamón[SUP] 11 [/SUP], Valentina Varela[SUP] 11 [/SUP], Carlos Batthyany[SUP] 9 [/SUP], Mariela Bollati-Fogolín[SUP] 12 [/SUP], Pablo Oppezzo[SUP] 13 [/SUP], Otto Pritsch[SUP] 2 10 [/SUP], José Luiz Proença-Módena[SUP] 6 [/SUP], Helder I Nakaya[SUP] 7 [/SUP], Emiliano Trias[SUP] 11 [/SUP], Luis Barbeito[SUP] 11 [/SUP], Ignacio Anegon[SUP] 14 [/SUP], María Cristina Cuturi[SUP] 14 [/SUP], Pedro Moraes-Vieira[SUP] 3 [/SUP], Mercedes Segovia[SUP] 1 2 [/SUP], Marcelo Hill[SUP] 1 2 [/SUP]



Affiliations

Abstract

Severe COVID-19 is associated with hyperinflammation and weak T cell responses against SARS-CoV-2. However, the links between those processes remain partially characterized. Moreover, whether and how therapeutically manipulating T cells may benefit patients are unknown. Our genetic and pharmacological evidence demonstrates that the ion channel TMEM176B inhibited inflammasome activation triggered by SARS-CoV-2 and SARS-CoV-2-related murine β-coronavirus. Tmem176b[SUP]-/-[/SUP] mice infected with murine β-coronavirus developed inflammasome-dependent T cell dysfunction and critical disease, which was controlled by modulating dysfunctional T cells with PD-1 blockers. In critical COVID-19, inflammasome activation correlated with dysfunctional T cells and low monocytic TMEM176B expression, whereas PD-L1 blockade rescued T cell functionality. Here, we mechanistically link T cell dysfunction and inflammation, supporting a cancer immunotherapy to reinforce T cell immunity in critical β-coronavirus disease.
 
Back
Top Bottom