Mast cells immune effectors

Chronic inflammatory response is one of the hallmarks of allergic diseases. Over the course of pollen season, there might be even a tenfold increase in numbers of nasal epithelial submucosal mast cells. Histamine released from these cells might not only induce acute allergic symptoms but also be crucial for sustaining this response into a chronic phase, as increasing evidence suggests that it influences several immune/inftammatory and effector functions (table 2) [2]. 

Grimbaldeston MA, Metz M, Yu M, Galli S J. 2006. Effector and potential immunoregulatory role of mast cells in IgE-mediated acquired immune responses. Curr Opin Immunol. 18 751-760. 

Thus, for the Hymenolepidids the data can be interpreted to fit the Th2 paradigm with the involvement of the predicted immune/ physiological effector mechanisms AB, complement, mast cells, eosinophils and goblet cells. 

Hapten-specific CD8+ T lymphocytes, likely the major effector population, are directly cytotoxic to chemical exposed keratinocytes and also release cytokines that boost the inflammatory response. In addition, Thl cells release a number of cytokines and chemokines that promote inflammation and activate mast cells and, in the presence of IFNy, are also capable of killing keratinocytes. Although the hapten may persist in skin for some time, this reaction is self-limited. CD4+ regulatory T cells that secrete IL-10 (similar to those described in relation to UV-induced immune suppression in Section 32.4.3) appear to play an important role in this regulation. 

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