[4][5] One of their unique abilities is that they suppress the innate and adaptive immune signals, making them important for regulating the inflammatory response.
[6] B10 cells predominantly localize in the spleen, though they are also found in the blood, lymph nodes, Peyer's patches, intestinal tissues, central nervous system, and peritoneal cavity.
[7] CD24, a human B10 marker, is exclusive to higher vertebrates and is absent in Vombatus and the organisms that diverged prior.
[3] When compared to the wild type or normal expression of antigen receptors, the B cells bound to CD19 molecules actually decreased inflammation.
[6] BCR-antigen interactions and BCR signaling facilitate antigen specificity and reactivity of B10 cells.
[3] These cognate interactions are dependent on MHC-II and CD40, and encourage IL-10 production and enable B10 cells to suppress macrophage function.
[1] In addition, their secretion of IL-10 can interfere with the phagocytosis, the activation of macrophages, and the production of cytokines and nitric oxide (NO).
[6] B10 cells have been studied in mouse models on account of their therapeutic relevance to autoimmune disease.
[3] In mouse models, the introduction of additional B10 cells during disease onset can mitigate and accelerate disease-related symptoms and progression.
[1] Moreover, B10 cell expansion in the absence of autoimmune-related production of inflammatory cytokine factors provides potential for immune response, allergy, and transplant rejection treatment.
[12] Their ability to promote cancer growth is attributed to immunosuppression mechanisms through innate and adaptive immune responses.
[1] The depletion of B10 cells enables a more rapid immune response and can improve pathogen clearance.