Mouse Homologue of Human HLA-DO Does Not Preempt Autoimmunity but Controls Murine Gammaherpesvirus MHV68.


Journal

Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R

Informations de publication

Date de publication:
15 12 2021
Historique:
received: 07 07 2021
accepted: 14 10 2021
pubmed: 24 11 2021
medline: 14 7 2022
entrez: 23 11 2021
Statut: ppublish

Résumé

H2-O (human HLA-DO) is a relatively conserved nonclassical MHC class II (MHCII)-like molecule. H2-O interaction with human HLA-DM edits the repertoire of peptides presented to TCRs by MHCII. It was long hypothesized that human HLA-DM inhibition by H2-O provides protection from autoimmunity by preventing binding of the high-affinity self-peptides to MHCII. The available evidence supporting this hypothesis, however, was inconclusive. A possibility still remained that the effect of H2-O deficiency on autoimmunity could be better revealed by using H2-O-deficient mice that were already genetically predisposed to autoimmunity. In this study, we generated and used autoimmunity-prone mouse models for systemic lupus erythematosus and organ-specific autoimmunity (type 1 diabetes and multiple sclerosis) to definitively test whether H2-O prevents autoimmune pathology. Whereas our data failed to support any significance of H2-O in protection from autoimmunity, we found that it was critical for controlling a γ-herpesvirus, MHV68. Thus, we propose that H2-O editing of the MHCII peptide repertoire may have evolved as a safeguard against specific highly prevalent viral pathogens.

Identifiants

pubmed: 34810225
pii: jimmunol.2100650
doi: 10.4049/jimmunol.2100650
pmc: PMC9124240
mid: NIHMS1749455
doi:

Substances chimiques

HLA-D Antigens 0
Histocompatibility Antigens Class II 0
Peptides 0
Receptors, Antigen, T-Cell 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2944-2951

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI117535
Pays : United States

Informations de copyright

Copyright © 2021 by The American Association of Immunologists, Inc.

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Auteurs

Jean Lee (J)

Committee on Cancer Biology, the University of Chicago, Chicago, IL.

Emily Cullum (E)

Committee on Immunology, the University of Chicago, Chicago, IL.

Kyle Stoltz (K)

Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI.

Niklas Bachmann (N)

Department of Microbiology, the University of Chicago, Chicago, IL.

Zoe Strong (Z)

Department of Pathology, the University of Chicago, Chicago, IL.

Danielle D Millick (DD)

Graduate School of Biomedical Sciences, Rutgers University, Piscataway, NJ.

Lisa K Denzin (LK)

Graduate School of Biomedical Sciences, Rutgers University, Piscataway, NJ.
Child Health Institute of New Jersey, Department of Pediatrics and Pharmacology, Rutgers Robert Wood Johnson Medical School, Rutgers, The State University of New Jersey, New Brunswick, NJ; and.

Anthony Chang (A)

Department of Pathology, the University of Chicago, Chicago, IL.

Vera Tarakanova (V)

Department of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI.

Alexander V Chervonsky (AV)

Committee on Immunology, the University of Chicago, Chicago, IL; tgolovki@bsd.uchicago.edu achervon@bsd.uchicago.edu.
Department of Pathology, the University of Chicago, Chicago, IL.
Committee on Microbiology, the University of Chicago, Chicago, IL.

Tatyana Golovkina (T)

Committee on Immunology, the University of Chicago, Chicago, IL; tgolovki@bsd.uchicago.edu achervon@bsd.uchicago.edu.
Department of Microbiology, the University of Chicago, Chicago, IL.
Committee on Microbiology, the University of Chicago, Chicago, IL.

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