Distribution of interleukin-2,-4,-10, tumour necrosis factor-α and transforming growth factor-β mRNAs in oral lichen planus

被引:105
作者
Simark-Mattsson, C [1 ]
Bergenholtz, G
Jontell, M
Eklund, C
Seymour, GJ
Sugerman, PB
Savage, NW
Dahlgren, UI
机构
[1] Univ Gothenburg, Dept Endodontol Oral Diag, Gothenburg, Sweden
[2] Univ Queensland, Dept Oral Biol & Pathol, Brisbane, Qld, Australia
[3] Univ Gothenburg, Dept Clin Immunol, Gothenburg, Sweden
关键词
cytokines; human; oral lichen planus; mononuclear leucocytes; T lymphocytes;
D O I
10.1016/S0003-9969(99)00013-8
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
In the present study. MRNA for the cytokines interleukin-2 (IL-2), IL-4, IL-10 tumour necrosis factor-alpha (TNF-alpha) and transforming growth factor beta-1 (TGF-beta-1) were investigated in oral lichen planus (OLP) lesions using in situ hybridization with S-35-labelled oligonucleotide probes on frozen tissue sections. In addition, the expression of interferon-gamma (IFN-gamma), IL-10 and IL-4 mRNAs was analysed in cultured lesional T lymphocytes from oral lichen planus by polymerase chain reaction. Cells expressing mRNA for IL-2, IL-4, IL-10, TNF-alpha and TGF-beta(1) were found in all the biopsies studied. Approximately 1-2% of the total number of infiltrating cells in the lesions were positive for each of the different cytokine mRNAs. Most biopsies contained basement membrane-oriented, mRNA-positive cells. In the cultured T-cell lines, message for IFN-gamma was detected in all the patients, IL-10 in all but one, and IL-4 in just one of the seven patients investigated. The results suggest that mRNA for both pro- and anti-inflammatory cytokines, i.e., mixed T-helper 1 (T(H)1) and T(H)2 cytokine profiles, are generated simultaneously by a limited number of cells in chronic lesions of OLP. (C) 1999 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:499 / 507
页数:9
相关论文
共 32 条
[1]   Th1-Th2: reliable paradigm or dangerous dogma? [J].
Allen, JE ;
Maizels, RM .
IMMUNOLOGY TODAY, 1997, 18 (08) :387-392
[2]   IMMUNOPATHOLOGICAL CHANGES IN THE SKIN FOLLOWING RECOMBINANT INTERLEUKIN-2 TREATMENT [J].
BLESSING, K ;
PARK, KGM ;
HEYS, SD ;
KING, G ;
EREMIN, O .
JOURNAL OF PATHOLOGY, 1992, 167 (03) :313-319
[3]   Transforming growth factor beta (TGF-beta)-dependent inhibition of T helper cell 2 (Th2)-induced autoimmunity by self-major histocompatibility complex (MHC) class II-specific, regulatory CD4(+) T cell lines [J].
Bridoux, F ;
Badou, A ;
Saoudi, A ;
Bernard, I ;
Druet, E ;
Pasquier, R ;
Druet, P ;
Pelletier, L .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (10) :1769-1775
[4]  
CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1016/0003-2697(87)90021-2
[5]  
CHU CQ, 1992, CLIN EXP IMMUNOL, V90, P522
[6]   NUMBER OF INTERLEUKIN-4-SECRETING AND INTERFERON-GAMMA-SECRETING HUMAN T-CELLS REACTIVE WITH TETANUS TOXOID AND THE MYCOBACTERIAL ANTIGEN PPD OR PHYTOHEMAGGLUTININ - DISTINCT RESPONSE PROFILES DEPENDING ON THE TYPE OF ANTIGEN USED FOR ACTIVATION [J].
ELGHAZALI, GEB ;
PAULIE, S ;
ANDERSSON, G ;
HANSSON, Y ;
HOLMQUIST, G ;
SUN, JB ;
OLSSON, T ;
EKRE, HP ;
TROYEBLOMBERG, M .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1993, 23 (11) :2740-2745
[7]   CONTACT SENSITIVITY AS A MODEL FOR T-CELL ACTIVATION IN SKIN [J].
ENK, AH ;
KATZ, SI .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1995, 105 (01) :S80-S83
[8]  
ENK AH, 1993, J IMMUNOL, V151, P2390
[9]  
FOX RI, 1994, J IMMUNOL, V152, P5532
[10]  
HERNANDEZPANDO R, 1994, IMMUNOLOGY, V82, P591