Expression Of TNF-α In Patients With Lichen Planus And The Relationship Between It And Lymphocyte Infiltrated

Lichen planus (LP) is a subacute or chronic inflammatory dermatosisinvolving skin and mucous membrane. LP takes it as the characteristic inpathology that stratum granulosum wedge proliferate, basal cells liquefactiondegenerate and lymphocytes infiltrate belt-shaped in the upper dermis. Tlymphocyte Accounts for the main proportion in the inflammatory soakage cell,generally 70-80%, mainly CD4+ and CD8+ T lymphocyte, which separatelyaccounts for the main proportion at the initial and later period. The pathogenesisisn't clear up to now. Most scholars believe that it relates to autoimmunization,mainly the immune response induced by T lymphocyte. In the process ofimmune response, cell factor plays an important role in regulating theintercellular mutual action, cell growth, cell differentiation and cell migration.TNF-α plays a key role in lymphocyte differentiation, activation,swimming, hastening, cytotoxic effect and so on. TNF-α has closedrelationship with inflammation, autoimmune diseases and so many kinds ofdiseases. TNF-α can be induced by endotoxin, virus, immune complex,neuropeptide matter P, IL-1,etc. TNF-α can be produced by many cells, suchas T lymphocyte, B lymphocyte, natural killing cell, endothelial cell, fibroblast,langerhans, keratinocyte, etc. TNF-α is very important in the cell toxic effect.TNF-α can induce cytotoxic T cell to differentiate, enhance monocytecytotoxic effect, stimulate lymph factor killing cell and natural killing cellactiveness. TNF-αcan induce endothelial cell and keratinocyte to form adhesivefactor and chemokines which plays the vital role in T cell migrating. TNF-α isthe center link in the cell factor network. Recently some authors extrapolate thatuniversal liquefaction and denaturalization of the basal cell in LP may beapoptosis caused by infiltrated lymphocyte. CD8+T cell may induce apoptosisthrough the following three kinds of mechanisms: T lymphocyte secretes TNF-α combining with TNFR of keratinocyte;The CD95L (FasL) of T lymphocytecombines with CD95 (Fas) of keratinocyte;T lymphocyte secretes granuleenzyme B that enters keratinocyte through the eyelet induced by porforin. Thesemechanisms cause keratinocyte apoptosis, activating enzyme associationresponse of keratinocyte cysteine containing aspartate specific protease.Although apoptosis gene has not yet been discovered directly through apoptosiscontrol, the accurate mechanism of apoptosis and anti-apoptosis is not clear,some apoptosis-related genes like TNF-α, Bcl-2, P53,Fas/FasL participate inthe development of LP. It is believed that in LP firstly the CD4+T lymphocyteactivates, then CD8+ T cell activates with the assistance of it;namely theextraneous source or endogenesis antigen is processed by antigen-presenting cell,then antigen is submitted to T lymphocyte which release certain cell factors,these factors can make T lymphocyte activate, multiply and wander to epidermis;Certain cell factors produced by T lymphocyte and cytotoxin T cell lead to thebasal cell destruction and damage, thereby causing the pathology and clinicalchanges of LP. The purpose of this paper is to investigate the expression ofTNF-α in patients with LP and discuss the relationship of lymphocyte withTNF-α, providing a certain basis for the pathogenesis and treatment of LP.Through searching literature it is found that TNF-α in wax pieces is examinedmainly by immunohistochemistry technology. In the experiments antigen hotrestoration and DAB staining are often used. This research used compoundenzyme and AEC staining in order to avoid taking off the phenomenon of a largenumber of pieces falling off and the interference induced by melanin granules.Methods: Sixty LP patients, diagnosed by clinic and histopathology, werecollected from the dermatological department of the Second Affiliated Hospitalof Jilin University from June, 2004 to December, 2006. The patients, 28 malesand 32 females, aged 9-72 years, with an average of 43.1,course from 20 days to3 years, had no other infective diseases and had not received any hormone andimmunotherapy during 2 recent months. Twenty normal skin specimens weretaken as normal controls collected from normal skin of operative patients inlaser hairdressing center attached to the dermatological department of theSecond Affiliated Hospital of Jilin University and the department of osteologyof China-Japan Union Hospital of Jilin University. The normal control, 8 malesand 12 females, aged 18-59 years, with an average of 37.7, had no otherinfective diseases and had not received any hormone and immunotherapy during2 recent years. There was no significant difference in sexes and ages betweenpatients and controls.The expression of TNF-α in patients with LP and normal skin wasexamined by immunohistochemistry SP, at the same time the lymphocytes werenumbered.Result evaluation: TNF-α expression: Observed under light microscope,cytoplasm/membrane positive staining was bright red. Cell counting wasperformed on five randomly selected high-power fields (×400),Classifiedaccording to positive cell rate: < 5% cell coloration was 0;5%-25% was 1;25%-50% was 2;> 50% was 3.Then classified according to positive cell shade:negative or unclear coloration was 0 minute;light red is 1;Red is 2;Bright redis 3. Both of two counts were plused: 0-1 was negative (-);2-3 was mild positive(+);4-5 was positive (++);> 5 was strong positive (+++).The lymphocytecounts: Randomly choosing five high-power fields from TNF-α positivespecimen (×400), the lymphocyte quantity was counted. The average wasobtained as relative quantity.SPSS 11.5 statistical software was used to handle the data.Results: The expression of TNF-α was found in 42 of 60 examples fromLP patients, rate was 72%. Positive staining mainly was located in the cellmembrane of spine cell, cytoplasm or membrane of lymphocyte. 20 examples ofnormal skin were negative. After statistics analysis, the expression of TNF-αwere difference between LP and normal skin, the difference was significant(P<0.01). TNF-α expression in the patients with LP had nothing to do with age,sex and course of illness, the difference were not significant ( P>0.05).ThroughSpearman rank correlation analysis, the expression of TNF-α and lymphocytenumber were positive correlation(γs=0.473,P<0.01).TNF-α can induce sensitive cell apoptosis, accelerate the expression ofadhesion molecule and chemokines which contribute to the transplanting andcongregating of lymphocyte. TNF-α can also induce cytotoxic T cell todifferentiate, enhance monocyte cytotoxic effect, stimulate lymph factor killingcell and natural killing cell activeness. In LP, the lymphocyte is the importantsource of TNF-α;at the same time TNF-α accelerates the expression ofadhesion molecule and chemokines which contribute to the transplanting andcongregating of lymphocytes, and the lymphocytes secrete TNF-α.Such of thecirculating mechanism may be the foundation of the LP chronic development.Conclusion: It is concluded that TNF-α plays a role in the pathogenesis ofLP. The expression of TNF-α and the number of lymphocyte were positivecorrelation. TNF-α induces lymphocyte to soakage, probably one of theimportant reasons for LP to take place and develop.