Mast cells: ontogeny, homing, and recruitment of a unique innate effector cell.
ABSTRACT Mast cells (MCs) are found principally in peripheral tissues yet are of bone marrow origin. Recent studies in mice trace the MC lineage from the common myeloid progenitor through the granulocyte-macrophage progenitor in the bone marrow to a committed MC progenitor (MCP). Additionally, at least in the mouse, a bipotent basophil-MC progenitor has been identified in the spleen, suggesting a physiologic role for this organ in MC development. MCPs are especially abundant in the mouse intestine, likely ensuring the capacity for a rapid expansion of MCs in the intestinal epithelium during the effector response to helminth infection and perhaps providing a pool of committed cells capable of redistribution to other tissues. Migration of MCPs to the intestine is constitutive and controlled by alpha chemokine receptor 2 and alpha4beta7 integrins expressed on the MCPs, with the latter integrin interacting with endothelial vascular cell adhesion molecule 1 and mucosal addressin cell adhesion molecule 1. In contrast, normal mouse lung tissue contains few MCPs and MCs, and these cellular reservoirs are not affected by the lack of alpha chemokine receptor 2 or alpha4beta7 integrin. Nonetheless, robust recruitment of MCPs to the lung occurs during experimentally induced allergic pulmonary inflammation and requires alpha4beta7 and alpha4beta1 integrins interacting with vascular cell adhesion molecule 1 but not with mucosal addressin cell adhesion molecule 1. Thus although MCs are present in all organs, the pathways responsible for the trafficking of MCPs from the circulation are organ specific and include both constitutive and inducible systems, ensuring both resident MCs and the potential for incremental recruitment in accord with the requirements of the immune response. These findings in mice await confirmation in human subjects.
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ABSTRACT: Mast cells (MCs) are implicated in the pathogenesis of allergic reactions and inflammatory conditions through the release of inflammatory mediators. So far limited attention has been given to the role of MCs in periodontitis. T cell immunoglobulin mucin domain (TIM)-3 is an immunomodulatory molecule and influences MC function. However, whether TIM-3 is expressed on MCs in the process of human periodontal disease has not been reported. Therefore, we identified MCs by toluidine blue staining and examined the expression of TIM-3 on tryptase-positive MCs in different severities of human chronic periodontitis using double-immunofluorescence staining in this study. A total of 83 human periodontal specimens were involved in this study, including healthy control tissues (n=25), chronic moderate periodontitis (n=28), and chronic severe periodontitis (n=30). The gingival specimens were fixed in 10% buffered formalin, stained with haematoxylin and eosin for histopathology, with toluidine blue for MCs, and with double-immunofluorescence for identification of tryptase-TIM-3 double-positive MCs in gingival tissues. Compared with healthy controls, the score of gingival tissue inflammation was significantly increased in the chronic moderate periodontitis (P=0.013) and chronic severe periodontitis (P<0.0001), and the densities (cells/mm(2)) of tryptase-TIM-3 double-positive MCs were significantly increased in both the chronic moderate (P=0.011) and severe periodontitis groups (P<0.0001). However, compared with the chronic moderate periodontitis group, both the score of gingival tissue inflammation (P=0.012) and the density of tryptase-TIM-3 double-positive MCs (P=0.011) in gingival tissue were significantly increased in the severe periodontitis groups. Significantly increased number of tryptase-TIM-3 double-positive MCs had the similar tendency as the severity of periodontitis inflammation in human chronic periodontitis. Our data suggest that TIM-3 may have a role on MCs in human chronic periodontitis.Archives of oral biology 04/2014; 59(6):654-661. · 1.65 Impact Factor
- Acta histochemica et cytochemica official journal of the Japan Society of Histochemistry and Cytochemistry 07/2014; · 1.22 Impact Factor
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ABSTRACT: We studied the effect of short-term activation of the maternal immune system with T-cell mitogen concanavalin A at the early terms of pregnancy on the postnatal development of the spleen in the offspring. It was found that single immunostimulatory exposure prior to the formation of the fetal immune system delays the postnatal development of the spleen until the beginning of puberty and impairs the formation of splenic lymphatic nodules with the predominant development of germinal centers as well as increases the number of mast cells in this organ.Bulletin of Experimental Biology and Medicine 02/2014; 156(4):509-11. · 0.34 Impact Factor