Thy-1+ epidermal cells in nude mice are distinct from their counterparts in thymus-bearing mice. A study of morphology, function, and T cell receptor expression.

We have evaluated the morphology, function, and TCR mRNA and DNA profiles of Thy-1+ epidermal cells (EC) derived from athymic (nude) mice. Based on these criteria we demonstrate that Thy-1+ EC in nude mice are predominantly round and angular and located in follicular epithelium, as compared to predominantly dendritic, interfollicular Thy-1+ EC found in normal CBA or BALB/c mice. Functionally, Thy-1+ EC from normal mice proliferate and elaborate IL-2 in response to stimulation by Con A; by contrast, nude Thy-1+ EC fail to proliferate or secrete IL-2 in response to Con A. Nude Thy-1+ EC proliferate markedly in response to low-dose IL-2 alone; Thy-1+ EC from normal mice give only modest proliferative responses to IL-2. Both populations of cells proliferate and elaborate IL-2 in response to PMA and calcium ionophore. Short-term cultured Thy-1+ EC from nude mice resemble Thy-1+ EC from normal animals in that they express no detectable functional TCR-alpha and beta-RNA. Normal Thy-1+ EC express abundant levels of functional RNA for TCR-gamma and delta-chains and for the CD3 delta-chain, whereas nude Thy-1+ EC produce no detectable TCR-delta and no CD3 delta-RNA and only truncated, presumably germ-line TCR-gamma transcripts, as suggested by lack of hybridization with gamma-V region probes and by lack of detectable rearrangements in the gamma-genes. These phenotypic, functional, and genotypic characteristics of Thy-1+ EC from nude mice suggest that these cells are at a very early stage of T cell differentiation.

Differential immune response of congenic mice to ultraviolet-treated major histocompatibility complex class II-incompatible skin grafts.

The influence of ultraviolet (UVB) irradiation on the survival of H-2 class II-disparate skin grafts was studied in congenic mouse strains. Isolated skin was UVB irradiated in vitro at a dose of 40 mJ/cm2 from both sides to remove Ia immunogenicity. Immediately after irradiation the skin was transplanted onto the flank of allogeneic mice. When B10.AQR grafts were transplanted onto B10.T(6R) recipients, a significant prolongation of the survival time was observed, while 50% of the UVB-treated grafts were not rejected at all. However, in the opposite direction--i.e., B10.T(6R) grafts onto B10.AQR recipients, no significant prolongation of the survival was observed. To test whether this effect was due to a difference in susceptibility of the donor skin to UVB irradiation or to a different immune response in the recipients, (B10.T(6R) x B10.AQR) grafts were transplanted onto the parent strains. Similar results were obtained, in that UVB-treated grafts did not show a prolonged survival in B10.AQR recipients, whereas a significant prolongation (50% of the grafts survived more than 100 days) was observed in B10.T(6R) recipients. UVB-treated (B10.T(6R) x B10.AQR)F1 grafts were also transplanted onto (B10.T(6R) x C57B1/10)F1, (B10.AQR x C57B1/10)F1, (B10.T(6R) x Balb/c)F1 and (B10.AQR x Balb/c)F1 recipients--but in none of these combinations was a prolonged survival time observed. These data suggest that, in contrast to all in vitro experiments, the abrogation of the immune response by UVB treatment of the stimulator cells is, in vivo, not a general phenomenon. The genetic constitution of the responder mice seems to play an important role in determining whether or not an immune response takes place.