Mast Cells: Bridging Host-Microorganism Interactions

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10 September 2021
Mast Cell Modulation of B Cell Responses: An Under-Appreciated Partnership in Host Defence
Alejandro M. Palma
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Jean S. Marshall
Evidence of cytokine and receptor-ligand interaction between mast cells and B cells has been depicted according to the following color scheme: red for evidence found in rodents, blue for evidence found in humans, and green for rodents and humans. Interaction between mast cells and B cells can occur at mucosal sites as well as at lymphoid and vascular tissues (although less frequently than at the mucosa). This is achieved by a broad array of cytokines (mainly type 2 cytokines, IL-10, IL-6, and IL-33), membrane-bound receptors and ligands (e.g., CD40/CD40L), and granule products such as histamine and proteases. These interactions can promote B cell proliferation, survival, class-switch to IgA or IgE, among other impacts. In addition, exosomes from both mast cells and B cells may be involved in communication between these cells. (Figure was prepared using BioRender).

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.

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Review
15 June 2021

Mast cells (MCs) are strategically located in tissues close to the external environment, being one of the first immune cells to interact with invading pathogens. They are long living effector cells equipped with different receptors that allow microbial recognition. Once activated, MCs release numerous biologically active mediators in the site of pathogen contact, which induce vascular endothelium modification, inflammation development and extracellular matrix remodeling. Efficient and direct antimicrobial mechanisms of MCs involve phagocytosis with oxidative and non-oxidative microbial destruction, extracellular trap formation, and the release of antimicrobial substances. MCs also contribute to host defense through the attraction and activation of phagocytic and inflammatory cells, shaping the innate and adaptive immune responses. However, as part of their response to pathogens and under an impaired, sustained, or systemic activation, MCs may contribute to tissue damage. This review will focus on the current knowledge about direct and indirect contribution of MCs to pathogen clearance. Antimicrobial mechanisms of MCs are addressed with special attention to signaling pathways involved and molecular weapons implicated. The role of MCs in a dysregulated host response that can increase morbidity and mortality is also reviewed and discussed, highlighting the complexity of MCs biology in the context of host-pathogen interactions.

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