Since alterations of epidermal Langerhans cells (LC) have been observed in humans infected with HIV, we investigated the morphology and function of these cells in
murine acquired immunodeficiency syndrome (
MAIDS), a murine model closely resembling human
AIDS. The number as well as the shape of dendritic MHC class II+ cells from ear skin of C57BL/6 mice were similar in normal and infected animals. In mixed epidermal cell (EC) lymphocyte cultures, EC from infected mice and from normal mice stimulated allogeneic T cell proliferation to the same extent. In contrast to T cells from normal mice, however, T cells from infected mice did not respond to allogeneic spleen cells, confirming the presence of a T-cell defect in
MAIDS.
Subcutaneous injection of syngeneic mice with trinitrophenyl-modified
MAIDS EC resulted in delayed ear swelling responses after challenge that were equivalent to those induced by
hapten-modified EC from normal mice, suggesting that the
contact sensitivity inducing potential of
MAIDS LC was preserved. To investigate
antigen presenting and processing function, EC and spleen cells were tested with the
ovalbumin-specific IAb-restricted T cell hybridoma BO.17.10 and either
ovalbumin 323-339
peptide or intact
ovalbumin protein.
MAIDS spleen cells had a reduced
antigen presenting capacity compared with normal spleen cells, whereas EC from these mice showed the same processing and presenting capacity as normal controls. In summary, our results demonstrate that the frequency, morphology, level of MHC
class II antigen expression and ability to process and present
antigen is normal for LC from mice with
MAIDS whereas the function of splenic T cells and APC from infected mice is significantly impaired.