Lymphocyte sub‐populations in the bladder wall in normal bladder, bacterial cystitis and interstitial cystitis

尿路上皮 粘膜下层 间质性膀胱炎 CD3型 单克隆抗体 CD8型 淋巴细胞 病理 医学 膀胱 免疫学 抗体 免疫系统 内科学 替代医学
作者
T. J. CHRISTMAS
出处
期刊:British journal of urology [Wiley]
卷期号:73 (5): 508-515 被引量:72
标识
DOI:10.1111/j.1464-410x.1994.tb07635.x
摘要

Objective To identify lymphocyte sub‐populations within the bladder wall in normal controls, in patients with bacterial cystitis (BC) or interstitial cystitis (IC). Patients and methods Bladder biopsies were taken from 21 patients with IC, four with BC and five normal controls. Immunofluorescent staining of biopsies was performed using monoclonal antibodies to the Tcell markers CD3, CD4, CD8, TCRδ1, δTCS1, βF1 and IML. Plasma cells were identified using monoclonal antibodies to IgA, IgG and IgM. The location and numbers of cells were determined. Peripheral blood lymphocyte counts were also performed in each case. Results T cells (CD4+ and CD8 +) were significantly more abundant within the bladder biopsies from patients with interstitial cystitis than in those from the normal controls, and were present within the urothelium and submucosa but not the detrusor. There was no difference between the numbers of T cells present in the biopsies from patients with interstitial cystitis and in those with bacterial cystitis. However, the presence of γδγ T cells was significantly associated with interstitial cystitis. IgA + and IgM + plasma cells were located within the urothelium and submucosa but not the detrusor in patients with IC and the numbers present in these patients were significantly greater than in those with BC or the normal controls. The peripheral blood lymphocyte counts were not altered in any of the study cases. Conclusion The increased numbers of CD4 +, CD8 + and γδ T cells as well as IgA +, IgG+ and IgM + plasma cells within the urothelium and submucosa in patients with IC suggest that these cells play an active role in the pathogenesis of the disorder. The previously described abnormal urothelial expression of HLA‐DR and hyperexpression of Class I molecules in patients with IC may enable these cells to cause destruction of the urothelium ‐ the end stage of IC.
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