The kinetics of cytokine gene expression in the thyroids of mice developing granulomatous experimental autoimmune thyroiditis

被引:26
作者
Tang, HW
Sharp, GC
Chen, KM
Braley-Mullen, H
机构
[1] Univ Missouri, Sch Med, Dept Internal Med, Columbia, MO 65212 USA
[2] Univ Missouri, Sch Med, Dept Mol Microbiol & Immunol, Columbia, MO 65212 USA
[3] Univ Missouri, Sch Med, Dept Pathol, Columbia, MO 65212 USA
[4] Dept Vet Affairs, Res Serv, Columbia, MO 65212 USA
关键词
autoimmunity; Th1/Th2; cytokine; in vivo animal models; CD8(+) T cells;
D O I
10.1006/jaut.1998.0247
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
To study the potential roles of cytokines in development and resolution of granulomatous experimental autoimmune thyroiditis (EAT), the kinetics of in vivo expression of cytokine genes in thyroid infiltrates was analysed using reverse transcriptase-PCR (RT-PCR). Both Th1 (IL-2 and IFN-gamma) and Th2 (IL-4 and IL-10) cytokines as well as TGF-beta, TNF-alpha, IL-12 and IL-1 beta were detected in thyroids during both the initial phase and peak of granulomatous EAT. Maximal expression of cytokine genes generally occurred 11-14 days after cell transfer, prior to maximal EAT severity, which occurred 19-21 days after cell transfer. The relative ratios of Th1:Th2 cytokines and mouse thyroglobulin-(MTg)-specific IgG1 and IgG2a autoantibody levels were similar during both the initial phase and peak of EAT. Depletion of CD8(+) T cells did not decrease the severity of EAT but delayed resolution of lesions. Cytokine gene expression in thyroids was not decreased by anti-CD8 treatment. Together, these data indicate that both Th1 and Th2 cytokines produced by CD4(+) T cells are involved in induction and development of granulomatous EAT, and CD8-dependent resolution of granulomatous EAT is apparently not mediated by these cytokines. (C) 1998 Academic Press.
引用
收藏
页码:581 / 589
页数:9
相关论文
共 47 条
[1]   Functional diversity of helper T lymphocytes [J].
Abbas, AK ;
Murphy, KM ;
Sher, A .
NATURE, 1996, 383 (6603) :787-793
[2]   IL-10 suppresses experimental autoimmune neuritis and down-regulates T(H)1-type immune responses [J].
Bai, XF ;
Zhu, J ;
Zhang, GX ;
Kaponides, G ;
Hojeberg, B ;
vanderMeide, PH ;
Link, H .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1997, 83 (02) :117-126
[3]   THE KINETICS OF CYTOKINE MESSENGER-RNA EXPRESSION IN THE RETINA DURING EXPERIMENTAL AUTOIMMUNE UVEORETINITIS [J].
BARTON, K ;
MCLAUCHLAN, MT ;
CALDER, VL ;
LIGHTMAN, S .
CELLULAR IMMUNOLOGY, 1995, 164 (01) :133-140
[4]  
Braley-Mullen H, 1998, AM J PATHOL, V152, P1347
[5]   INDUCTION OF SEVERE GRANULOMATOUS EXPERIMENTAL AUTOIMMUNE-THYROIDITIS IN MICE BY EFFECTOR-CELLS ACTIVATED IN THE PRESENCE OF ANTI-INTERLEUKIN-2 RECEPTOR ANTIBODY [J].
BRALEYMULLEN, H ;
SHARP, GC ;
BICKEL, JT ;
KYRIAKOS, M .
JOURNAL OF EXPERIMENTAL MEDICINE, 1991, 173 (04) :899-912
[6]   INDUCTION OF EXPERIMENTAL AUTOIMMUNE-THYROIDITIS IN MICE WITH INVITRO ACTIVATED SPLENIC T-CELLS [J].
BRALEYMULLEN, H ;
JOHNSON, M ;
SHARP, GC ;
KYRIAKOS, M .
CELLULAR IMMUNOLOGY, 1985, 93 (01) :132-143
[7]   REGULATION OF THE INDUCTION AND RESOLUTION OF GRANULOMATOUS EXPERIMENTAL AUTOIMMUNE-THYROIDITIS IN MICE BY CD8(+) T-CELLS [J].
BRALEYMULLEN, H ;
MCMURRAY, RW ;
SHARP, GC ;
KYRIAKOS, M .
CELLULAR IMMUNOLOGY, 1994, 153 (02) :492-504
[8]   Treatment of experimental encephalomyelitis with a peptide analogue of myelin basic protein [J].
Brocke, S ;
Gijbels, K ;
Allegretta, M ;
Ferber, I ;
Piercy, C ;
Blankenstein, T ;
Martin, R ;
Utz, U ;
Karin, N ;
Mitchell, D ;
Veromaa, T ;
Waisman, A ;
Gaur, A ;
Conlon, P ;
Ling, N ;
Fairchild, PJ ;
Wraith, DC ;
OGarra, A ;
Fathman, CG ;
Steinman, L .
NATURE, 1996, 379 (6563) :343-346
[9]   IMMUNE-MECHANISMS IN AUTOIMMUNE-THYROIDITIS [J].
CHARREIRE, J .
ADVANCES IN IMMUNOLOGY, 1989, 46 :263-+
[10]  
Chen K C, 1981, J Appl Toxicol, V1, P127, DOI 10.1002/jat.2550010213