The phenotype and function of CD1a(+) lymph cells is of considerable intere
st. By means of microsurgical lymph cannulation human lymph derived from no
rmal skin was sampled. Cells were isolated and processed for immunocytochem
istry, electron microscopy, flow cytometry and functional assays. The major
ity of the cells, (62%), were T cells. The other cells comprised CD1a(+) ce
lls (7%), monocytes/macrophages (8%), and B cells (1%); the remainder were
erythrocytes or uncharacterized cells. The CD1a(+) cells reacted with antib
odies against protein S-100, HLA-DR, the Lag antigen, CD4, CD11a, CD11b, CD
18, CD25, CD40, CD54, CD80 and CD86. Interestingly, a small prolow portion
the of CD1a(+) cells (about 5%) reacted with an antibody to CD14. The CD1a(
+) cells did not react with an antibody against human follicular dendritic
cells nor were they CD19-, CD23-, E-cadherin- or factor XIIIa-positive. Bot
h allogenic and antigen-specific T cell proliferation stimulated by antigen
-presenting lymph cells were strongly inhibited by adding anti-CD80 and ant
i-CD86 antibodies. By electron microscopy Birbeck granules were detected in
only 22% of the CD1a(+) lymph cells and these cells exhibited an extensive
ruffling of the surface. These findings demonstrate that CD1a(+) lymph cel
ls, which do not express the dermal dendritic cell marker factor XIIIa, res
emble dendritic cells formerly designated as 'veiled' as well as lymphoid d
endritic cells, suggesting that after migration to the regional lymphoid or
gans, Langerhans cells form a more differentiated population of dendritic c
ells specialized in sensitizing T lymphocytes. Our results add further supp
ort to the view that resident Langerhans cells may be precursors of lymphoi
d dendritic cells acquiring the final phenotype in the microenvironment of
the lymph node.