| Literature DB >> 31751612 |
Pasqualina De Leo1, Luisa Gazzurelli2, Manuela Baronio2, Davide Montin3, Silvia Di Cesare4, Carmen Giancotta4, Francesco Licciardi3, Caterina Cancrini4, Alessandro Aiuti5, Alessandro Plebani2, Maria Pia Cicalese6, Vassilios Lougaris2, Georgia Fousteri7.
Abstract
Mutations affecting the non-canonical pathway of NF-κB were recently identified to underlie a form of common variable immunodeficiency strongly associated with autoimmunity. Although intrinsic B-cell abnormalities explain most of the humoral defects of this disease, detailed data on the impact of NFKB2 on follicular helper (Tfh) and regulatory (Tregs) T cells are scarce. Here, we show that Tfh, CXCR5+, and CXCR5- Treg cell subsets were significantly reduced in patients heterozygous for a truncating mutation of NFKB2. Plasma CXCL13 levels were reduced, underlining an important role for NFKB2 in regulating the germinal center (GC) response. Proinflammatory IFNγ, IL-17 and IL-10 cytokine production by CD4 T cells was lower in the mutated patients, but the production of IL-4 and IL-21 was not altered. Taken together, our findings show that NFKB2 influences the quality and efficiency of human GC reaction, by affecting not only the B cells but also GC-relevant T cell subsets.Entities:
Keywords: Common variable immunodeficiency (CVID); Follicular helper T cells (Tfh); Follicular regulatory T cells (Tfr); NFKB2; T regulatory cells (Treg)
Year: 2019 PMID: 31751612 DOI: 10.1016/j.clim.2019.108309
Source DB: PubMed Journal: Clin Immunol ISSN: 1521-6616 Impact factor: 3.969