Abstract
Close physical proximity between mast cells and T cells has been demonstrated in several T cell mediated inflammatory processes such as rheumatoid arthritis and sarcoidosis. However, the way by which mast cells are activated in these T cell-mediated immune responses has not been fully elucidated. We have identified and characterized a novel mast cell activation pathway initiated by physical contact with activated T cells, and showed that this pathway is associated with degranulation and cytokine release. The signaling events associated with this pathway of mast cell activation have also been elucidated confirming the activation of the Ras mitogen-activated protein kinase systems. More recently, we hypothesized and demonstrated that mast cells may also be activated by microparticles released from activated T cells that are considered as miniature version of a cell. By extension, microparticles might affect the activity of mast cells, which are usually not in direct contact with T cells at the inflammatory site. Recent works have also focused on the effects of regulatory T cells (Treg) on mast cells. These reports highlighted the importance of the cytokines IL-2 and IL-9, produced by mast cells and T cells, respectively, in obtaining optimal immune suppression. Finally, physical contact, associated by OX40–OX40L engagement has been found to underlie the down-regulatory effects exerted by Treg on mast cell function.
Highlights
Most commonly known for their role in the elicitation of IgEmediated allergic inflammation, mast cells have been implicated in a range of other non-allergic inflammatory processes
Both in vitro and in vivo studies have demonstrated that mast cells or their products are pivotal in mediating leukocyte recruitment into inflammatory sites, are capable of presenting antigens to T cells, interact directly with and affect the function of cells of the adaptive immune system, and mediate tissue remodeling (Mekori, 2004; Bachelet et al, 2006; Kalesnikoff and Galli, 2008; Dudeck et al, 2011)
By using W/W v mice reconstituted with mast cells obtained from TNF−/− mice, it could be shown in vivo that TNF-α and MIP-2 were essential for appropriate neutrophil recruitment during T cell-induced cutaneous delayed hypersensitivity reactions
Summary
Most commonly known for their role in the elicitation of IgEmediated allergic inflammation, mast cells have been implicated in a range of other non-allergic inflammatory processes. Both murine and human mast cells could be activated to both release granule-associated mediators, such as histamine and matrix metalloproteinase-9 (MMP-9), and to produce several cytokines (i.e., TNF-α, IL-4, IL-6, and IL-8) upon physical contact with activated, but not resting, T cells (Inamura et al, 1998; Baram et al, 2001; Salamon et al, 2005, 2008).
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