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Review
. 2024 Apr 4:15:1360296.
doi: 10.3389/fimmu.2024.1360296. eCollection 2024.

MASTer cell: chief immune modulator and inductor of antimicrobial immune response

Tomás Alejandro Suárez Vázquez  1 , Nallely López López  1 , Mario César Salinas Carmona  1
Affiliations
Review

MASTer cell: chief immune modulator and inductor of antimicrobial immune response

Tomás Alejandro Suárez Vázquez et al. Front Immunol. .

Abstract

Mast cells have long been recognized for their involvement in allergic pathology through the immunoglobulin E (IgE)-mediated degranulation mechanism. However, there is growing evidence of other "non-canonical" degranulation mechanisms activated by certain pathogen recognition receptors. Mast cells release several mediators, including histamine, cytokines, chemokines, prostaglandins, and leukotrienes, to initiate and enhance inflammation. The chemical nature of activating stimuli influences receptors, triggering mechanisms for the secretion of formed and new synthesized mediators. Mast cells have more than 30 known surface receptors that activate different pathways for direct and indirect activation by microbes. Different bacterial strains stimulate mast cells through various ligands, initiating the innate immune response, which aids in clearing the bacterial burden. Mast cell interactions with adaptative immune cells also play a crucial role in infections. Recent publications revealed another "non-canonical" degranulation mechanism present in tryptase and chymase mast cells in humans and connective tissue mast cells in mice, occurring through the activation of the Mas-related G protein-coupled receptor (MRGPRX2/b2). This receptor represents a new therapeutic target alongside antibiotic therapy. There is an urgent need to reconsider and redefine the biological role of these MASTer cells of innate immunity, extending beyond their involvement in allergic pathology.

Keywords: bacterial infections; degranulation; immunomodulation; innate immunity; mast cell.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Figures

Figure 1
Figure 1
Activation mechanism of mast cells. Canonic: (A) FcϵRI, high-affinity IgE receptor; (B) METS, mast cell extracellular traps; (C) phagocytosis; (D) ROS, reactive oxygen species; (E) TLR2, Toll-like receptor; (F) MRGPRX2/b2, Mas-related G protein–coupled receptor; (G) FcγRs, Fc-gamma receptor for IgG; (H) C3aR/C5aR complement receptors.
Figure 2
Figure 2
Mast cell modulates innate and adaptative immunity. Innate immunity: (A) neutrophil, (B) monocyte, and (C) dendritic cell. Adaptative immunity: (D) CD4 lymphocyte, (E) CD8 lymphocyte, and (F) B lymphocyte.
See this image and copyright information in PMC

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