In vivo description of dendritic cells in human renal cell carcinoma

Citation
T. Schwaab et al., In vivo description of dendritic cells in human renal cell carcinoma, J UROL, 162(2), 1999, pp. 567-573
Citations number
39
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
JOURNAL OF UROLOGY
ISSN journal
00225347 → ACNP
Volume
162
Issue
2
Year of publication
1999
Pages
567 - 573
Database
ISI
SICI code
0022-5347(199908)162:2<567:IVDODC>2.0.ZU;2-#
Abstract
Purpose: Dendritic cells (DCs) are efficient and effective antigen-presenti ng cells that play a major role in initiating the primary immune response. They are the most potent stimulators of T-cell activation and would thus be expected to be of great importance in the antitumoral immune response. Alt hough DC phenotype and function have been described under in vitro conditio ns, their in vivo characteristics are less well detailed. Human renal cell carcinoma (RCC) is an excellent model to explore tumor infiltrating dendrit ic cells (TiDCs) because of rare clinical spontaneous regressions and the a ssociation of high numbers of tumor infiltrating lymphocytes (TiLs), sugges ting a strong immune response. Materials and Methods: We determined the in situ phenotype of mature CD83() TiDCs using monoclonal antibodies to known activation molecules (CD86 [B7 .2], CD80 [B7.1], CD40, CD54, CD1a and HLA-DR). Seventeen primary RCCs, rep resenting four distinct histologies, were evaluated using double-staining i mmunohistochemical techniques and light microscopy. Results: CD83(+) TiDCs were found in all tumors. Expression of CD40 correla ted with expression of CD1a on CD83(+) TiDCs. Expression of CD54 (ICAM-1) c orrelated with a lower expression of CD86 (B7.2) as well as a decrease in C D3(+) and CD8(+) TiLs. Conclusions: These data suggest a de novo lipid or sugar-based immunogenic antigen presentation by TiDCs. Also, the data support an impaired antigen-p resenting capability for CD54(+) TiDCs based on the decreased coexpression of CD86 (B7.2) and the decrease of associated CD8(+) TiLs.