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Lymphocyte sub‐populations in the bladder wall in normal bladder, bacterial cystitis and interstitial cystitis
Author(s) -
CHRISTMAS T. J.
Publication year - 1994
Publication title -
british journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 0007-1331
DOI - 10.1111/j.1464-410x.1994.tb07635.x
Subject(s) - urothelium , submucosa , interstitial cystitis , cd3 , monoclonal antibody , cd8 , lymphocyte , pathology , medicine , urinary bladder , immunology , antibody , immune system , alternative medicine
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.