Abstract
Mast cells are well known to be activated via cross-linking of immunoglobulins bound to surface receptors. They are also recognized as key initiators and regulators of both innate and adaptive immune responses against pathogens, especially in the skin and mucosal surfaces. Substantial attention has been given to the role of mast cells in regulating T cell function either directly or indirectly through actions on dendritic cells. In contrast, the ability of mast cells to modify B cell responses has been less explored. Several lines of evidence suggest that mast cells can greatly modify B cell generation and activities. Mast cells co-localise with B cells in many tissue settings and produce substantial amounts of cytokines, such as IL-6, with profound impacts on B cell development, class-switch recombination events, and subsequent antibody production. Mast cells have also been suggested to modulate the development and functions of regulatory B cells. In this review, we discuss the critical impacts of mast cells on B cells using information from both clinical and laboratory studies and consider the implications of these findings on the host response to infections.
Highlights
The ability of mast cells to aid in the initiation and regulation of acquired immune responses has been demonstrated by multiple authors [1,2,3,4,5,6]
As shown by various reports [139, 140], Candida spp. can induce IgE-mediated mast cell degranulation and subsequent responses in humans who have been previously sensitised and both promote inflammation and exacerbate histaminergic symptoms of patients. These findings suggest a dual role of mast cells in the interaction with Candida spp.: they act as sentinels and first line of defence, but their mediators can become detrimental for the host and perpetuate inflammation
B cells in the skin have often been overlooked but both B1 and B2 cells are present and B cell populations in these sites are increased during inflammation
Summary
The ability of mast cells to aid in the initiation and regulation of acquired immune responses has been demonstrated by multiple authors [1,2,3,4,5,6]. Human mast cells from several tissues including the airways express OX40L [39], and this has been shown to provide a mechanism whereby mast cells may promote T cell responses. Expression levels of OX40/OX40L and CD40/CD40L were elevated Inhibition of these pathways decreases the levels of OVA-specific IgA and IgE and reduces antigen-dependent mediator-release by mast cells. This model shows how B cells are activated by mast cells through the CD40/ CD40L pathway as well as the OX40/OX40L-axis, in the presence of appropriate cytokines such as IL-4, IL-13, IL-6, and TGF-b. Given the wide range of cell types expressing these molecules it may be a more general method to regulate immune responses in certain tissues
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