Regulation of Decay Accelerating Factor Primes Human Germinal Center B Cells for Phagocytosis.

Dernstedt A, Leidig J, Holm A, Kerkman PF, Mjösberg J, Ahlm C, Henriksson J, Hultdin M, Forsell MNE

Front Immunol 11 (-) 599647 [2021-01-05; online 2021-01-05]

Germinal centers (GC) are sites for extensive B cell proliferation and homeostasis is maintained by programmed cell death. The complement regulatory protein Decay Accelerating Factor (DAF) blocks complement deposition on host cells and therefore also phagocytosis of cells. Here, we show that B cells downregulate DAF upon BCR engagement and that T cell-dependent stimuli preferentially led to activation of DAFlo B cells. Consistent with this, a majority of light and dark zone GC B cells were DAFlo and susceptible to complement-dependent phagocytosis, as compared with DAFhi GC B cells. We could also show that the DAFhi GC B cell subset had increased expression of the plasma cell marker Blimp-1. DAF expression was also modulated during B cell hematopoiesis in the human bone marrow. Collectively, our results reveal a novel role of DAF to pre-prime activated human B cells for phagocytosis prior to apoptosis.

Bioinformatics Compute and Storage [Service]

PubMed 33469456

DOI 10.3389/fimmu.2020.599647

Crossref 10.3389/fimmu.2020.599647

pmc: PMC7813799


Publications 8.1.0