The effects of B-cell-activating factor on the population size, maturation and function of murine natural killer cells

Quah, PS; Sutton, V; Whitlock, E; Figgett, WA; Andrews, DM; Fairfax, KA; Mackay, F

Author(s): Quah, PS; Sutton, V; Whitlock, E; Figgett, WA; Andrews, DM; Fairfax, KA; Mackay, F;
Details: Publication Year 2022-11,Volume 100,Issue #10,Page 761-776
Journal Title: Immunology & Cell Biology
Publication Type: Research article
Abstract: The role of B-cell-activating factor (BAFF) in B-lymphocyte biology has been comprehensively studied, but its contributions to innate immunity remain unclear. Natural killer (NK) cells form the first line of defense against viruses and tumors, and have been shown to be defective in patients with systemic lupus erythematosus (SLE). The link between BAFF and NK cells in the development and progression of SLE remains unstudied. By assessing NK cell numbers in wild-type (WT), BAFF(-/-) (BAFF deficient), BAFF-R(-/-) (BAFF receptor deficient), TACI(-/-) (transmembrane activator and calcium modulator and cyclophilin ligand interactor deficient), BCMA(-/-) (B-cell maturation antigen deficient) and BAFF transgenic (Tg) mice, we observed that BAFF signaling through BAFF-R was essential for sustaining NK cell numbers in the spleen. However, according to the cell surface expression of CD27 and CD11b on NK cells, we found that BAFF was dispensable for NK cell maturation. Ex vivo and in vivo models showed that NK cells from BAFF(-/-) and BAFF Tg mice produced interferon-gamma and killed tumor cells at a level similar to that in WT mice. Finally, we established that NK cells do not express receptors that interact with BAFF in the steady state or in the BAFF Tg mouse model of SLE. Our findings demonstrate that BAFF has an indirect effect on NK cell homeostasis and no effect on NK cell function.
Keywords: Mice; Animals; *Transmembrane Activator and CAML Interactor Protein/genetics; Population Density; *Lupus Erythematosus, Systemic; Interleukin-4; Mice, Transgenic; Killer Cells, Natural/metabolism; Autoimmunity; Cancer; Immunodeficiency; Innate immunity; Natural killer cell
Department(s): Laboratory Research
PubMed ID: 36106449
Publisher's Version: https://doi.org/10.1111/imcb.12585
Open Access at Publisher's Site: https://doi.org/10.1111/imcb.12585
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 2025-03-07 02:36:20

Last Modified: 2025-03-07 02:38:23