Abstract
Mast cells are well accepted as important sentinel cells for host defence against selected pathogens. Their location at mucosal surfaces and ability to mobilize multiple aspects of early immune responses makes them critical contributors to effective immunity in several experimental settings. However, the interactions of mast cells with viruses and pathogen products are complex and can have both detrimental and positive impacts. There is substantial evidence for mast cell mobilization and activation of effector cells and mobilization of dendritic cells following viral challenge. These cells are a major and under-appreciated local source of type I and III interferons following viral challenge. However, mast cells have also been implicated in inappropriate inflammatory responses, long term fibrosis, and vascular leakage associated with viral infections. Progress in combating infection and boosting effective immunity requires a better understanding of mast cell responses to viral infection and the pathogen products and receptors we can employ to modify such responses. In this review, we outline some of the key known responses of mast cells to viral infection and their major responses to pathogen products. We have placed an emphasis on data obtained from human mast cells and aim to provide a framework for considering the complex interactions between mast cells and pathogens with a view to exploiting this knowledge therapeutically. Long-lived resident mast cells and their responses to viruses and pathogen products provide excellent opportunities to modify local immune responses that remain to be fully exploited in cancer immunotherapy, vaccination, and treatment of infectious diseases.
Highlights
Mast cells (MC) are strategically placed at sites that interface with our external environment such as the skin, lung, and intestines
In vitro infection of human MCs with dengue was highly antibody-dependent and occurred through an FcγRII-dependent mechanism [40]. This could suggest that the major contribution of MCs in response to human dengue virus (DENV) infection might be in the context of secondary infections that are associated with more severe disease
RV infection of both primary MCs and MC lines is limited by pre-exposure of the cells to IFNβ [11]. This latter finding is in keeping with evidence that IFNβ production is deficient in asthmatics who show increased susceptibility to respiratory viral infection. These findings suggest a role for MCs in enhancing asthma exacerbations and having a proinflammatory impact in response to RV
Summary
Mast cells (MC) are strategically placed at sites that interface with our external environment such as the skin, lung, and intestines. Within such tissues they are predominately below the epithelial layer and closely associated with blood vessels This location allows them to act as sentinels for tissue damage and pathogen invasion. The association between MC and blood vessels is optimal to enhance the rapid recruitment of effector cells out of the bloodstream and into neighboring tissues This process is facilitated by the MC’s rapid production of cytokine mediators such as TNF and IL-1β that activate endothelium, lipid mediators that facilitate vasodilatation, as well as a range of chemokines that promote the selective recruitment of specific subsets of effector cells. Understanding effective host responses to infection is critical for defining MC activation signals and responses by which immunity could be enhanced or inhibited in disease settings
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