NK cell spatial dynamics and IgA responses in gut-associated lymphoid tissues during SIV infections.


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
07 07 2022
Historique:
received: 20 06 2021
accepted: 22 06 2022
entrez: 7 7 2022
pubmed: 8 7 2022
medline: 12 7 2022
Statut: epublish

Résumé

HIV infection induces tissue damage including lymph node (LN) fibrosis and intestinal epithelial barrier disruption leading to bacterial translocation and systemic inflammation. Natural hosts of SIV, such as African Green Monkeys (AGM), do not display tissue damage despite high viral load in blood and intestinal mucosa. AGM mount a NK cell-mediated control of SIVagm replication in peripheral LN. We analyzed if NK cells also control SIVagm in mesenteric (mes) LN and if this has an impact on gut humoral responses and the production of IgA known for their anti-inflammatory role in the gut. We show that CXCR5 + NK cell frequencies increase in mesLN upon SIVagm infection and that NK cells migrate into and control viral replication in B cell follicles (BCF) of mesLN. The proportion of IgA+ memory B cells were increased in mesLN during SIVagm infection in contrast to SIVmac infection. Total IgA levels in gut remained normal during SIVagm infection, while strongly decreased in intestine of chronically SIVmac-infected macaques. Our data suggest an indirect impact of NK cell-mediated viral control in mesLN during SIVagm infection on preserved BCF function and IgA production in intestinal tissues.

Identifiants

pubmed: 35798936
doi: 10.1038/s42003-022-03619-y
pii: 10.1038/s42003-022-03619-y
pmc: PMC9262959
doi:

Substances chimiques

Immunoglobulin A 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

674

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI143457
Pays : United States
Organisme : Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)
ID : R01AI143457

Informations de copyright

© 2022. The Author(s).

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Auteurs

Philippe Rascle (P)

Institut Pasteur, Unité HIV Inflammation and Persistance, Université de Paris, Paris, France.
Université Paris Diderot, Sorbonne Paris Cité, Paris, France.

Cyril Planchais (C)

Institut Pasteur, Laboratory of Humoral Immunology, Université de Paris, Paris, France.
INSERM U1222, Paris, France.

Béatrice Jacquelin (B)

Institut Pasteur, Unité HIV Inflammation and Persistance, Université de Paris, Paris, France.

Marie Lazzerini (M)

Institut Pasteur, Unité HIV Inflammation and Persistance, Université de Paris, Paris, France.

Vanessa Contreras (V)

CEA, Université Paris Sud 11, INSERM U1184, Immunology of Viral Infections and Autoimmune Diseases, IDMIT, IBFJ, Fontenay-aux-Roses, France.

Caroline Passaes (C)

Institut Pasteur, Unité HIV Inflammation and Persistance, Université de Paris, Paris, France.

Asier Saez-Cirion (A)

Institut Pasteur, Unité HIV Inflammation and Persistance, Université de Paris, Paris, France.

Hugo Mouquet (H)

Institut Pasteur, Laboratory of Humoral Immunology, Université de Paris, Paris, France.
INSERM U1222, Paris, France.

Nicolas Huot (N)

Institut Pasteur, Unité HIV Inflammation and Persistance, Université de Paris, Paris, France.

Michaela Müller-Trutwin (M)

Institut Pasteur, Unité HIV Inflammation and Persistance, Université de Paris, Paris, France. mmuller@pasteur.fr.

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