Answers are grounded in this paper and cite their sources.
This articlc reviews the clinical and laboratory aspects of the relationship between atopy and dermatophytosis. This newly appreciated relationship; chronic, stabilized dermatophytosis and bronchial asthma and/or allergic rhinitis, constitutes a clinical syndrome of importance and interest. The relevant host defense; correlate, cell mediated immunity, is subject to the modulating effects of the mediators of Immunoglobulin-E mediated hypersensitivity in the atopic. Evidence suggests that lgE, the mast cell and histamine act locally within the loose connective tissue of the skin to inhibit T effector cell function and inflammation. The final common pathway for histamine as an immune modulator is unknown but may involve binding to H-2 receptors on the plasma membrane of lymphocytes or endothelial cells. The consequent reduction in intensity of inflammation within the lesion permils establishment of a chronic stabilized dermatophyte infection. Recognition of the atopic-chronic-dermatophytosis syndrome draws attention to the underlying immune mechanism which may have broader implications in biology.
No takes yet. Share an insight, caveat, or question.
Henry E. Jones (1980) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: