Shared transcriptional profiles of atypical B cells suggest common drivers of expansion and function in malaria, HIV, and autoimmunity.


Journal

Science advances
ISSN: 2375-2548
Titre abrégé: Sci Adv
Pays: United States
ID NLM: 101653440

Informations de publication

Date de publication:
05 2021
Historique:
received: 30 01 2021
accepted: 07 04 2021
entrez: 27 5 2021
pubmed: 28 5 2021
medline: 28 5 2021
Statut: epublish

Résumé

Chronic infectious diseases have a substantial impact on the human B cell compartment including a notable expansion of B cells here termed atypical B cells (ABCs). Using unbiased single-cell RNA sequencing (scRNA-seq), we uncovered and characterized heterogeneities in naïve B cell, classical memory B cells, and ABC subsets. We showed remarkably similar transcriptional profiles for ABC clusters in malaria, HIV, and autoimmune diseases and demonstrated that interferon-γ drove the expansion of ABCs in malaria. These observations suggest that ABCs represent a separate B cell lineage with a common inducer that further diversifies and acquires disease-specific characteristics and functions. In malaria, we identified ABC subsets based on isotype expression that differed in expansion in African children and in B cell receptor repertoire characteristics. Of particular interest, IgD

Identifiants

pubmed: 34039612
pii: 7/22/eabg8384
doi: 10.1126/sciadv.abg8384
pmc: PMC8153733
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).

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Auteurs

Prasida Holla (P)

Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA.

Brian Dizon (B)

National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA.

Abhijit A Ambegaonkar (AA)

Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA.

Noga Rogel (N)

Department of Pathology, Sackler School of Medicine, Tel Aviv University, Israel.

Ella Goldschmidt (E)

Department of Pathology, Sackler School of Medicine, Tel Aviv University, Israel.

Arun K Boddapati (AK)

NIAID Collaborative Bioinformatics Resource, National Institutes of Health, Bethesda, MD, USA.

Haewon Sohn (H)

Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA.

Dan Sturdevant (D)

RML Genomics Unit, Research Technologies Section, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.

James W Austin (JW)

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Lela Kardava (L)

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Li Yuesheng (L)

National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.

Poching Liu (P)

National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.

Susan Moir (S)

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Susan K Pierce (SK)

Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA. asafmadi@gmail.com spierce@nih.gov.

Asaf Madi (A)

Department of Pathology, Sackler School of Medicine, Tel Aviv University, Israel. asafmadi@gmail.com spierce@nih.gov.

Classifications MeSH