Prostatitis Home
IPCN3 Home
Search
How to view videos
Abstracts from meeting
Meeting attendees
It works for me
Prostatitis Foundation
Archives

Third International Chronic Prostatitis Network

The immunopathology of Chronic Pelvic Pain Syndrome–Type IIIa


A. Doble, M.M. Walker, R.O’N. Witherow, J.R.W. Harris, D. Taylor-Robinson, L.W. Poulter
Department of Urology, Addenbrookes Hospital, Cambridge,
Departments of Urology and Sexually Transmitted Diseases, St. Mary’s Hospital, London and
Department of Immunology, Royal Free Hospital, London, UK
Introduction & Objectives
Chronic Pelvic Pain Syndrome (CPPS) Type IIIa is a poorly understood condition with little data on the underlying immunopathology. Ultrasound guided biopsy and the use of panels of monoclonal antibodies have enabled characterisation of the pheno-type of the inflammatory population and postulation of the immunopathological mechanisms.
Methods
Prostatic biopsy material obtained under ultrasound guidance from 24 patients with CPPS Type IIIa and 10 controls was subjected to immunohistochemical analysis. A panel of monoclonal antibodies (RFDR-HLA DR, RFT mix-pan leucocyte, CD4-helper T lymphocytes, CD8-suppressor/cytotoxic T lymphocytes, RFB mix-B lymphocytes, RFD1-antigen presenting cells, RFD7-tissue macrophages, CD7- activated T lymphocytes) was used to define the inflammatory cell phenotype.
Results
In controls faint HLA DR expression (MHC class II antigen) was observed in basal epithelial cells and a scanty T cell distribution with equal numbers of CD4 and CD 8 lymphocytes. There were no B cells and only scanty members of the monocyte/macrophage series. In type IIIa patients HLA DR expression was most marked in glandular structures increasing in intensity with inflammatory grade severity. T cell numbers increased with the degree of inflammation, with CD8 cells becoming increasingly prominent. With advancing inflammatory grade the number of antigen-presenting cells and mature tissue macrophages increased as did the proportion of activated CD8 lymphocytes. The same pattern was not observed with the CD4 subset.
CONCLUSION
The inflammatory cell phenotype can be compared with inflammatory conditions whose immunopathology is defined. The pattern observed in type IIIa prostatitis is cell mediated. The antigen-presenting cell distribution and CD4/CD8 lymphocyte ratio is more in keeping with a persistent antigenic presence rather than immunoregulatory dysfunction, as seen in rheumatoid arthritis.
© 2002 The Prostatitis Foundation
Further Contact:(click on words or mailbox)

This page was created by Ideasmith®.

Add to this site