T CELL - PRODUCED ANTIGEN - BINDING FACTOR ANALOGOUS TO IgE

Delayed-type hypersensitivity skin reactions are mediated by recirculating, sensitized Ly-I ÷ T cells (1, 2) that enter the tissues and are activated by specific antigen. This leads to the release of various nonspecific macromolecular mediators (lymphokines) that attract various leukocytes to leave the circulation and enter the tissues to comprise a characteristic infiltrate of inf lammatory cells. In mice, this cellular recrui tment requires that the activated T cells also activate resident tissue mast cells to release the vasoactive amine serotonin, which causes gaps to form between vascular endothelial cells (3 6). This allows the leukocytes to emigrate into the extravascular tissue spaces in response to chemat t rac tant lymphokines (5, 6). The fact that T cell-dependent act ivation of mast cells is required for elicitation of delayed-type hypersensitivity led us to investigate whether a T cell product could mimic some of the functions of immunog lobu l in E (IgE) ant ibody. We have described (7) a T cell-derived an t igen-b ind ing factor that transfers an immedia te hypersensitivity-like reaction. In the present study this T cell factor was compared with a hybr idoma |gE antibody. Both transferred sensitization for elicitation of immediatetype skin reactions with accompanying vascular permeabili ty. Neither was active in mast cell-deficient mice. The T cell factor was distinguished from IgE by a n u m b e r of immunochemica l and biological properties; inc luding affinity chromatography using specific ant i -IgE and anti-factor antibodies, and a shorter dura t ion of passive sensitization. The T cell factor is a suitable candida te for par t ic ipat ion in the mechanism by which T cells activate mast cells in delayed-type hypersensitivity.