DELAYED-TYPE HYPERSENSITIVITY IN MAST CELL-DEFICIENT MICE - DEPENDENCE ON PLATELETS FOR EXPRESSION OF CONTACT SENSITIVITY

Previous studies of cutaneous T cell-mediated responses in mice have o btained pharmacologic, morphologic, and immunologic evidence pointing to a critical role for local mast cells in release of the vasoactive a mine serotonin (5-HT) to mediate early, initiating events that are req uired for elicitation of these responses. However, the role of mast ce lls in initiating these T cell-mediated cutaneous responses has been q uestioned due to the presence of relatively intact delayed-type hypers ensitivity responses, such as contact sensitivity (CS), in mast cell-d eficient mice whose skin contains only 1% normal mast cell numbers. Th e contribution of other potential local sources of 5-HT, such as circu lating platelets, at the site of a delayed-type hypersensitivity or CS response in these mast cell-deficient strains, has not been investiga ted. Therefore, we studied the effect of systemic platelet depletion, produced with an anti-platelet Ab, on blood and tissue levels of 5-HT, and on in vivo T cell-mediated cutaneous sensitivity responses, in W/ W-v and SI/SId mast cell-deficient mice. The results showed that: 1) p latelet depletion severely reduced whole blood 5-HT; 2) tissue levels of 5-HT, in mast cell-deficient mice, depended in large part on the pr esence of circulating platelets, and 3) specific depletion of platelet s markedly suppressed CS responses in both W/W-v and SI/SId mast cell- deficient mice, and only moderately reduced CS in normal +/+ congenic mast cell-sufficient controls, but did not decrease CS in beige mice, with platelet granules that are defective in storage of 5-HT. We concl uded that platelets may provide 5-HT crucial for the initiation of cut aneous T cell-mediated immune responses, such as CS.