Toll-like receptor 7 (TLR7)-driven accumulation of a novel CD11c⁺ B-cell population is important for the development of autoimmunity.
Blood, 2011/8/04;118(5):1305-15.
Rubtsov AV[1], Rubtsova K, Fischer A, Meehan RT, Gillis JZ, Kappler JW, Marrack P
Affiliations
PMID: 21543762DOI: 10.1182/blood-2011-01-331462
Impact factor: 25.476
Abstract
Females are more susceptible than males to many autoimmune diseases. The processes causing this phenomenon are incompletely understood. Here, we demonstrate that aged female mice acquire a previously uncharacterized population of B cells that we call age-associated B cells (ABCs) and that these cells express integrin α(X) chain (CD11c). This unexpected population also appears in young lupus-prone mice. On stimulation, CD11c(+) B cells, both from autoimmune-prone and healthy strains of mice, secrete autoantibodies, and depletion of these cells in vivo leads to reduction of autoreactive antibodies, suggesting that the cells might have a direct role in the development of autoimmunity. We have explored factors that contribute to appearance of ABCs and demonstrated that signaling through Toll-like receptor 7 is crucial for development of this B cell population. We were able to detect a similar population of B cells in the peripheral blood of some elderly women with autoimmune disease, suggesting that there may be parallels between the creation of ABC-like cells between mice and humans.
MeSH terms
Aged; Aging; Animals; Autoimmune Diseases; Autoimmunity; B-Lymphocyte Subsets; B-Lymphocytes; CD11c Antigen; Case-Control Studies; Cell Proliferation; Cells, Cultured; Female; Humans; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Toll-Like Receptor 7
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