Dense accumulation of mononuclear cells (lymphocytes >> macrophages) in the
dermal-epidermal interface and a T cell-mediated cytotoxic reaction agains
t basal keratinocytes are hallmarks of lichen planus lesions. In this study
, we focused on the chemotactic signals responsible for the selective recru
itment of these cells. Using in situ hybridization and immunohistochemistry
, the expression and localization of the lymphocyte-and/or monocyte/macroph
age-attractant CC chemokines macrophage chemoattractant protein-1 (MCP-1),
regulated on activation, normal T cell expressed, and secreted (RANTES), ma
crophage inflammatory protein-la and -1 beta (MIP-1 alpha/beta), I-309 and
the CXC chemokines monokine induced by interferon-gamma (MIG), interferon-g
amma-inducible protein-10 interleukin-8 (IL-8), epithelial-derived neutroph
il attractant-78, and growth-related oncogene-alpha were investigated, Stro
ng mRNA expression of MIG, IP-10, and MCP-1 and moderate mRNA expression of
RANTES and MIP-la were detected exclusively within foci characterized by s
trong infiltration with CD3(+) lymphocytes (CD4(+) cells > CD8(+) cells) an
d CD68(+) macrophages. All other chemokines investigated were minimally exp
ressed or absent. With more than 11% of total cells strongly expressing MIG
transcripts, this selectively lymphotactic chemokine was by far the domina
nt chemokine and thus may significantly contribute to the inflammatory reac
tion in lichen planus lesions. According to the mRNA expression profiles, M
IG, IP-10, and MCP-1 were expressed by both basal keratinocytes above and m
ononuclear cells within the inflammatory foci, Our findings indicate that a
set of chemokines composed of IP-10, MCP-1, RANTES, MIP-1 alpha, and espec
ially MIG contributes to the cytokine network and preferential trafficking
of mononuclear cells to the interface region off lichen planus lesions.