The Correlated Study On Expression Of Intercellular Adhesion Molecule-1 In Cutaneous Lichen Planus

Background: Lichen planus (LP) is also called lichen ruber planus, it is a chronic or subacute inflammatory disease of the skin and mucous membrane. The skin lesions are often mauve , polygonal, flat papulas accompanied with pruritus, occasionally with hypertrophic plaques, erosions or bullas. Pigmentation often remained after the regression of the lesions. Both male and female can be affected. The etiological factor and pathogenesis have not yet been finalized. Intercellular Adhesion Molecule-1( ICAM-1) is a kind of transmembrane glycoproteins as a ligand for lymphocyte function assotiated antigen-1(LFA-1). It participates inflammatory and graft rejective reactions. Current domestic and foreign study found that T Cell-mediated immune reaction participates the pathogenetic course of LP, meanwhile ICAM-1 can enhance the activation and proliferation of T lymphocytic cells, therefore, the author speculates that ICAM-1 may participate lymphocytic infiltration and activation in the skin lesion of LP , and eventually leading to the distinctive pathological changes.Objective: To study the expression of ICAM-1 antigen on lesional keratinocytes in LP, and its relationship with the dermal infiltrating lymphocytes.Methods: 30 specimens of the lesion tissue of LP patients diagnosed by both clinic and biopsy were chosen as experimental guoup, control specimens were 10 normal skin tissue obtained during esthetic surgical procedures. serial paraffin sections of these specimens and streptavidin-peroxidase complex (SP) immunohisto--chemical staining was performed. The staining slides were observed under light microscope, meanwhile the number of related cells was counted. Statistical comparison was made using the analysis of Fisher's exact test for numeration variables. Correlation between the expression level of ICAM-1 in keratinocytes and the number of infiltrating lymphocytes in the dermis was analyzed by Spearman's rank correlation test. The significant level of both tests was P= 0.05.Results: 1. Among the normal specimens , ICAM-1 expression was not found. but it was found among most of the experimental specimens(23/30). The stained area was in the cytoplasm and at the cell membrane. Most of the stained cells were observed in the prickle cell layer and basal layer . The reaction between ICAM-1 and its monoclonal antibody was enhanced in the vascular endothelial cells in the dermis. And positive expression of the infiltrating lymphocytes in the dermis can also be found.2. Spearman's rank correlation test was applied to analyse the correlation between the expression level of ICAM-1 in the lesional keratinocytes and the number of infiltrating lymphocytes in the dermis. The coefficient correlation(r_s)=0.368, and P=0.11>0.05, so there was not statistically significant correlation between them.Discussion: Currently many immunology research found that T Cell-mediated immune reaction participates the pathogenetic course of LP. This study found among the normal specimens , ICAM-1 expression was negative. But among most of the experimental specimens(23/30), it was positive .The stained area was in the cytoplasm and at the cell membrane. most of the stained cells were observed in the prickle cell layer and basal layer .The reaction between ICAM-1 and its monoclonal antibody was enhanced in the vascular endothelial cells in the dermis. and positive expression of the infiltrating lymphocytes in the dermis can also be found. The upregulation of ICAM-1 in the lesional keratinocytes can be analyzed as follows:①Various exotic stimuli , including chemicals, ultraviolet light (UV)and infection of bacteria or virus etc. can induce the production of several pro-inflamatary mediators by keratinocytes, such as the cytokines of tumour necrosis factor-alpha(TNF-alpha)or interleukin-l(IL-l), by which one or several information transduction pathways were activated. then the activation of the protein kinase followed. subsequently, the nuclear factor-kappaB (NF-κB)was activated and moved into the cytoplasm, then it combined with the kappaB sequence in the ICAM-1 gene, and mediated the transcription and expression of the ICAM-1 gene eventually.②The cytokines released from infiltrating lymphocytes in the dermis and the epidermotropic lymphocytes can also promote the expression of ICAM-1. Correlation between the expression level of ICAM-1 in keratinocytes and the number of infiltrating lymphocytes in the dermis was analyzed by Spearman's rank correlation test. there was not statistically significant correlation between them. this can be explained as follows:①The expression of ICAM-1 didn't rely on the numbers of the infiltrating lymphocytes in considerable extent. the keratinocytes could be activated directly by the stimuli of ultraviolet, micromolecule and other detriment factors, and secret cytokines , then expressed the ICAM-1 antigen. The ICAM-1 expressed through the non-antigen-depended pathway was also quite important. ?There was a sophisticated regulating process in the expression of ICAM-1,when the number of dermal infiltrating lymphycytes was in Certain range, the upregulation was developed. but when the number exceeded certain extent , it might initiate some mechanism, and the expression was limited. but this mechanism needs to be verified by further studies.Conclusion:1. The ICAM-1 antigen was not expressed in the epidermis of normal skin , but it was obviousely expressed by the lesional keratinocytes of LP. 2. The expression of ICAM-1 in the lesional keratinocytes didn't depend on the numbers of the infiltrating lymphocytes completely, and it might participate the process of the antigen presentation , the activation and homing of T lymphcytes and the apoptosis of the basal cells. eventually the infiltrating lymphocytes zone in the upper dermis and the liquefactive degeneration of the basal cells were developed.