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From the SRHI (CEA,DSV-DRM),*
Commissariat à
l’Energie Atomique; the Institut de Recherche sur la
Peau,
Hôpital Saint-Louis; and the
Unité de Dermatologie,
Hôpital
Tenon (Ap-Hp), Paris, France
Recent data have suggested that in psoriasis, the
T-infiltrating cells could be submitted to regulatory pathways,
possibly through natural killer receptors. HLA-G binds to different
natural killer receptors and is able to inhibit T-cell functions.
Because this molecule is induced by interferon-
, a major
cytokine in psoriasis, we asked whether HLA-G and its receptor
might be expressed in this disease. Specific RNAs for HLA-G1 and HLA-G5
were consistently found in lesional skin specimens, soluble
HLA-G5 transcripts being found only in psoriasis. HLA-G protein was
found in all psoriatic sections, but never in normal skin
controls. Double labeling demonstrated that HLA-G-positive cells were
CD68+, CD11c+ macrophages. The NKR ILT2
was also present in psoriatic skin, the T
CD4+-infiltrating cells expressing indeed ILT2. The
demonstration of HLA-G and ILT2 expression in psoriatic skin suggests
that this pathway may act as an inhibitory feed back aimed to
down-regulate the deleterious effects of T-cell infiltrate in this
disease.
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