Th2 dominance in nasal mucosa in patients with Wegener's granulomatosis

被引:57
作者
Balding, CEJ
Howie, AJ
Drake-Lee, AB
Savage, COS [1 ]
机构
[1] Univ Birmingham, Sch Med, MRC Ctr Immune Regulat, Div Med Sci,Renal Immunobiol Lab, Birmingham B15 2TT, W Midlands, England
[2] Univ Birmingham, Sch Med, Dept Pathol, Birmingham B15 2TT, W Midlands, England
[3] Univ Hosp, ENT Dept, Birmingham, W Midlands, England
关键词
cytokines; kidney; vasculitis;
D O I
10.1046/j.1365-2249.2001.125002332.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Wegener's granulomatosis initially affects upper respiratory tract organs including the nasal mucosa in more than 90% of patients. The inflammation is typically granulomatous with associated vasculitis. T lymphocytes are usually a prominent component of the leucocyte infiltrate. Previous studies using peripheral blood T cells have implicated IFN-gamma rich Th1-type responses. This study addressed the cytokine milieu in nasal mucosa from 10 patients with active Wegener's granulomatosis using immunohistochemistry. Increased levels of CD3(+) T cells and eosinophils were present compared with normal and disease controls. There was increased expression of IL-4, down-regulation of IL-2 and no detectable IFN-gamma. There was increased expression of the chemokine receptor CCR3 by infiltrating cells, consistent with an IL-4 dominant, Th2-biased response. In contrast, renal biopsy tissue from 10 patients with active Wegener's granulomatosis showed expression of IL-2 and IL-4. The Th2-type environment within nasal mucosa, often the initial site of disease activity in Wegener's, is consistent with a local allergic response in these patients.
引用
收藏
页码:332 / 339
页数:8
相关论文
共 21 条
[1]  
BROUWER E, 1994, CLIN EXP IMMUNOL, V98, P448
[2]   Interleukin-8: A pathogenetic role in antineutrophil cytoplasmic autoantibody-associated glomerulonephritis [J].
Cockwell, P ;
Brooks, CJ ;
Adu, D ;
Savage, COS .
KIDNEY INTERNATIONAL, 1999, 55 (03) :852-863
[3]   Glycosaminoglycans contribute to multiple functions of vascular endothelial cells [J].
Cockwell, P ;
Adams, DH ;
Savage, COS .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1996, 104 (01) :1-3
[4]  
Csernok E, 1999, ARTHRITIS RHEUM, V42, P742, DOI 10.1002/1529-0131(199904)42:4<742::AID-ANR18>3.3.CO
[5]  
2-9
[6]  
Cunningham MA, 1999, J AM SOC NEPHROL, V10, P499
[7]   ANTIMYELOPEROXIDASE ANTIBODIES STIMULATE NEUTROPHILS TO DAMAGE HUMAN ENDOTHELIAL-CELLS [J].
EWERT, BH ;
JENNETTE, JC ;
FALK, RJ .
KIDNEY INTERNATIONAL, 1992, 41 (02) :375-383
[8]  
GODMAN GC, 1954, AMA ARCH PATHOL, V58, P533
[9]   WEGENER GRANULOMATOSIS AUTOANTIBODIES IDENTIFY A NOVEL DIISOPROPYLFLUOROPHOSPHATE BINDING-PROTEIN IN THE LYSOSOMES OF NORMAL HUMAN-NEUTROPHILS [J].
GOLDSCHMEDING, R ;
VANDERSCHOOT, CE ;
HUININK, DT ;
HACK, CE ;
VANDENENDE, ME ;
KALLENBERG, CGM ;
VONDEMBORNE, AEGK .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 84 (05) :1577-1587
[10]   T cell responses to myeloperoxidase (MPO) and proteinase 3 (PR3) in patients with systemic vasculitis [J].
Griffith, ME ;
Coulthart, A ;
Pusey, CD .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1996, 103 (02) :253-258