| Lichen Planus (LP) is a chronic inflammatory mucocutaneous disease of unknown etiology and pathogenesis. It is characterized path-ologically by basal cell damage associated with the infiltration of lym-phocytes in the upper dermis. The formation of colloid bodies in the lower epidermis and upper dermis is observed most commonly in LP. The previous studies indicated that globulin, complement and fibrin, colloid bodies deposit at the dermo-epidermal junction of LP. Olsens etc. found lichen planus specific antibody ( LPSA) in epidermis, which was also found in patients' serum . All these suggested LP was related with humoral immune. Recently, with application of immuno-histochemistry and in situ hybridization on the research of infiltrated cell in the LP lesion, most of the researchers identified LP is chronic, cell-mediated immune damage to basal keratinocytes. Colloid bodies are apoptotic keratinocytes. Helper T lymphocyte ( Th) is predomi-nant infiltrated cell in the superior dermis, while cytotoxic T lympho-cyte ( Tc) , Langerhans cell and monocyte in the epidermis. Current researches suppose that LP is a delayed-type hypersensitivity response to an unidentified antigen, which activate Langerhans cells, then shape and number of Langerhans cells changed and cytokines excre-ted, which can attract more T lymphocyte infiltrate. T lymphocyte is activated, excretes more cytokines. These cytokines can induce theexpression of disorder antigens on the keratinocyte and accelerate T lymphocyte adhere with these keratinocytes. Then Tc damages the ke-ratinocytes, which leads to basal cell destruction at last.CD43 ( Leukosialin/sialophorin) molecule is a cell adhesion mol-ecule with heavily glycosylated transmembrane protein, CD43 expres-ses on the surface of most hemopoietic cells. Its gene locates in 16pll. 2. Previous studies indicated that CD43 have many kinds of bi-ology functions: Inducing adherence and anti-adherence between cells; Participating in the growth, activation, hyperplasia and apopto-sis of immunocyte; Participating in signal conduction and adjusting the gene expression in the immunocyte; Adjusting T lymphocyte homing and recirculating; Adjusting conversion of antibody type of B lympho-cyte (IgM ?IgG) ; Participating in inflammation reaction and forma-tion of arteriosclerosis and so on. Recently, CD43 are found related with connective tissue disease, psoriasis, AIDS, skin tumor etc.To study the expression of CD43 and the association of CD43 with infiltrated Ivmphocvtes in LP lesion, Immunohistochemical studv wasperformed on biopsies from 32 patients with LP and 30 examples of normal persons using a panel of monoclonal antibody ( CD43, CD3, CD4, CD8, CD20) on formalin -fixed, paraffin -embedded tissue sec-tions.Material1. Trial object;Trial group: 32 examples of patients finally diagnosed by clinical and pathology.Control group: 30 examples of normal person skin.2. Reagent: mouse antihuman CD43, CD3, CDS, CD20 McAb, Histostain?Plus Kits (Zymed corporation, USA), mouse antihuman CD4 McAb (NOVA corporation, United Kingdom). Poly-L-Lysine, ImM EDTA (PH8.0) solution, DAB kit from Beijing Zhongshan liv-ing technological company.3. Equipment: Finesse 325 microtome (German Thermo Shan-don company) ; constant temperature oven ( Shen Yang medical appa-ratus factory); BX410LMPUS light microscope (Japan OLMPUS company) ; LG microwave oven.Method1. Cleaning carry sheet glass;2. Preparing formalin-fix, paraffin-embedded tissue sections;3. Immunochemical staining;4. Counterstaining with hematoxylin, sealing the pieces with Canada gum;5. Counting under microscope;6. Using Metamorph Imaging System V4. 6 computer image anal-ysis software (UIC corporation , USA) to measures CD43 dying inten-sity ;7. Data are analysised by SPSS12. 11 software.Results1. Keratinocytes and the derma inflammation cells in LP lesions all can express CD43 molecule. The CD43+ keratinocytes are chiefly found in the early stage lesions (P < 0.0... |
PDF Full Text Request