A close-up on the expanding landscape of CD21-/low B cells in humansShow others and affiliations
2022 (English)In: Clinical and Experimental Immunology, ISSN 0009-9104, E-ISSN 1365-2249, Vol. 210, no 3, p. 217-229Article, review/survey (Refereed) Published
Abstract [en]
Memory B cells (MBCs) are an essential part of our immunological memory. They respond fast upon re-encountering pathogens and can differentiate into plasma cells that secrete protective antibodies. The focus of this review is on MBCs that lack, or express low levels of, CD21, hereafter referred to as CD21-/low. These cells are expanded in peripheral blood with age and during chronic inflammatory conditions such as viral infections, malaria, common variable immunodeficiency, and autoimmune diseases. CD21-/low MBCs have gained significant attention; they produce disease-specific antibodies/autoantibodies and associate with key disease manifestations in some conditions. These cells can be divided into subsets based on classical B-cell and other markers, e.g. CD11c, FcRL4, and Tbet which, over the years, have become hallmarks to identify these cells. This has resulted in different names including age-associated, autoimmune-associated, atypical, tissue-like, tissue-resident, tissue-restricted, exhausted, or simply CD21-/low B cells. It is however unclear whether the expanded 'CD21-/low' cells in one condition are equivalent to those in another, whether they express an identical gene signature and whether they have a similar function. Here, we will discuss these issues with the goal to understand whether the CD21-/low B cells are comparable in different conditions.
Place, publisher, year, edition, pages
Oxford University Press, 2022. Vol. 210, no 3, p. 217-229
Keywords [en]
CD21-, low, memory B cells, exhaustion, age-associated, atypical, autoimmune-associated
National Category
Immunology in the medical area
Research subject
Infection Biology
Identifiers
URN: urn:nbn:se:his:diva-22206DOI: 10.1093/cei/uxac103ISI: 000910668700001PubMedID: 36380692OAI: oai:DiVA.org:his-22206DiVA, id: diva2:1731068
Funder
Swedish Research Council, 2018-03128Swedish Research Council, 2021-01150Swedish Research Council, 2016-00288Swedish Rheumatism Association, R-94129Swedish Rheumatism Association, R-940945Swedish Cancer Society, 19 0464Swedish Childhood Cancer Foundation, PR2018-0170
Note
CC BY 4.0
Correspondence: Inga-Lill Mårtensson, Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg 40530, Sweden. Email: lill.martensson@rheuma.gu.se
Received 19 July 2022; Revised 5 October 2022; Accepted for publication 14 November 2022
Funding has been received from: the Swedish Research Council 2018-03128 and 2021-01150 (ILM), 2016-00288 (IG), the Patient Association for Rheumatic Diseases R-94129 (ILM), R-940945 (IG), the Swedish Cancer Foundation 19 0464 (ILM), the Childhood Cancer Foundation PR2018-0170 (ILM), and the ALF agreement between the Swedish government and the county councils ALFGBG-965435 (IG), ALFGBG-277797 (ILM).
2023-01-262023-01-262023-05-03Bibliographically approved