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Low ICAM‐1 expression in the epidermis of depigmenting C57BL/6J‐mi vit /mi vit mice: A possible cause of muted contact sensitization
Author(s) -
Nordlund James J.,
Csato Miklos,
Babcock George,
Takei Fumio
Publication year - 1995
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.1995.tb00217.x
Subject(s) - epidermis (zoology) , sensitization , chemistry , microbiology and biotechnology , medicine , biology , immunology , anatomy
The depigmenting C57BL/6J‐mi vit /mi vit ) (mi vit /mi vit ) 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 mi vit /mi vit epidermal cells. In the mi vit /mi vit mice, however, only subcutaneous injection of haptcnizcd C57BL/6 epidermal cells caused an immune response. The response of these mi vit /mi vit mice 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 mi vit /mi vit epidermal cells can process and present and mi vit /mi vit T lymphocytes can react to the antigen. We postulated the presence of a deficient in vivo interaction between epidermal cells and T lymphocytes in the mi vit /mi vit mice. ICAM‐I is an important adhesion signal regulating epidermal cell/T‐lymphocyte interaction. Us expression in mi vit /mi vit mice was studied using YN1/1 antibody against MALA‐2, the murine counterpart of human ICAM‐1. In contrast to C57BL/6 animals, the mi vit /mi vit epidermis essentially did not stain with the antibody after hapten challenge. In vitro after stimulation with TPA or IFN‐γ, the mi vit /mi vit epidermal cells expressed significantly lesser amounts of ICAM‐1 than the C57BL/6 epidermal cells. Lower expression of ICAM‐1 by mi vit mi vit /mi vit sol;mi vit epidermal cells has also been demonstrated both by direct staining and by flow cytomelry. The binding of lymphocytes to mi vit /mi vit epidermal 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 mi vit /mi vit mice at least partly results from lower expression of ICAM‐1 and thus defective epidermal ccll/T‐lymphocyte interaction.