Several mast cell-derived mediators, when tested individually, have actions that may be considered immunosuppressive or anti-inflammatory. Yet evidence concerning the importance of mast cells to the down regulation of T cell-dependent immune responses in vivo is scanty and contradictory. To test directly the net contribution of intact mast cells to the suppression of delayed hypersensitivity reactions in vivo, we attempted to elicit tolerance to contact sensitivity in W/W(v) or S1/S1(d) mast cell-deficient mice, and compared their responses with those of littermate control mice with normal numbers of mast cells. By using three different measures of delayed hypersensitivity (ear swelling, weight ratios of challenged and control ears, and 125I-IUDR-labeled leukocyte infiltration into challenged and controls ears), we detected no deficiency in the 24 hr contact sensitivity reactions to DNFB in control (nontolerized) W/W(v) or S1/S1(d) mice. We thus confirmed previous work indicating that mast cells are not essential for the induction and elicitation of delayed hypersensitivity. Furthermore, mast cell-deficient and control mice developed equivalent levels of tolerance to contact sensitivity. This was true for tolerance induced by DNBS administered i.v. 7 days before epicutaneous sensitization with DNFB, and for tolerance induced by supraoptimal sensitization with DNFB. W/W(v) and S1/S1(d) mice also served as suitable donors and recipients for putative suppressor T cells (Ts) induced by i.v. DNBS. We conclude that mast cells make little or no contribution to the modulation of Ts activity in two different models of Ts-dependent tolerance to contact sensitivity.
|Number of pages||7|
|Journal||Journal of Immunology|
|State||Published - 1985|