AbstractThe depigmenting C57BL/6J‐mivit/mivit) (mivit/mivit) mouse, a congenic mutant of the C57BL/6 strain, exhibits an isolated, single immune deficiency. It is unable to mount a normal immune/inflammatory response upon epicutaneous application of DNFB or TNCB, although it does respond normally to oxazalone. The present investigtions have been carried out to further study this deficiency.In vivo, C57BL/6 mice could be sensitized by the epicutaneous application of the hapten TNCB, the subcutaneous injection of haplen(TNBS)‐conjugated C57BL/6, and hapten conjugated mivit/mivitepidermal cells. In the mivit/mivitmice, however, only subcutaneous injection of haptcnizcd C57BL/6 epidermal cells caused an immune response. The response of these mivit/mivitmice could be documented only by adoptive transfer of splenic lymphocytes into naive C57BL/6 animals which then reacted to challenge doses of TNCB. These observations suggest that mivit/mivitepidermal cells can process and present and mivit/mivitT lymphocytes can react to the antigen. We postulated the presence of a deficient in vivo interaction between epidermal cells and T lymphocytes in the mivit/mivitmice. ICAM‐I is an important adhesion signal regulating epidermal cell/T‐lymphocyte interaction. Us expression in mivit/mivitmice was studied using YN1/1 antibody against MALA‐2, the murine counterpart of human ICAM‐1. In contrast to C57BL/6 animals, the mivit/mivitepidermis essentially did not stain with the antibody after hapten challenge.In vitroafter stimulation with TPA or IFN‐γ, the mivit/mivitepidermal cells expressed significantly lesser amounts of ICAM‐1 than the C57BL/6 epidermal cells. Lower expression of ICAM‐1 by mivitmivit/mivitsol;mivitepidermal cells has also been demonstrated both by direct staining and by flow cytomelry. The binding of lymphocytes to mivit/mivitepidermal monolayers, which were stimulated to express ICAM‐1 by IFN‐y, was decreased compared to that of C57BL/6 epidermal cells. We conclude that the muted contact sensiliza‐tion response detected in vivo in the mivit/mivitmice at least partly results from lower expression of ICAM‐1 and thus defective epidermal ccl