Figure 4.

Physical contact between mast cells and T cells/eosinophils. Mast cells and activated T cells in the inflammation site can perform physical contact (heterotypic adhesion) mediated by adhesion molecules (i. e. ICAM-1 [on mast cells], LFA-1 [on T cells]), thereby being activated to release inflammation-related mediators (histamine, TNFα, MMP-9, interleukin, metallopeptidase inhibitor 1, etc.). Heterotypic adhesion also shows that mast cells have a broad ability to directly mediate T cell activation. In addition, mast cells can be activated by microvesicles released by T cells that carry activating factors, responding to the site of inflammation without contact with T cells. Mast cells and eosinophils have been observed in the late and chronic stages of allergic inflammation to regulate each other’s functions by forming an effect unit. CD48 (on mast cells) and CD244 (on eosinophils), DNAM-1 (on mast cells), and Nectin-2 (on eosinophils) have been reported to mediate this effect. ECP, eosinophil cationic protein; PAF, platelet-activating factor; MMP-9, matrix metalloproteinase-9; IFN-λ1, interferon-λ1; EPO, eosinophil peroxidase; MBP, major basic protein; VEGF, vascular endothelial growth factor; SCF, stem cell factor; TSLP, thymic stromal lymphopoietin; TNFα, tumor necrosis factor α; TF, tissue factor; ICAM-1, intercellular adhesion molecule-1; LFA-1, leukocyte function-related antigen-1; DNAM-1, DNAX accessory molecule 1.