IL-10 is highly expressed in the cryptorchid cryptepididymal epithelium: A probable mechanism preventing immune responses against autoantigenic spermatozoa in the epididymal tubule

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Abstract

The expression of several immunoregulatory adhesion proteins and cytokines was studied in the normal epididymis, cryptorchid cryptepididymis, the epididymis of oestrogen-treated mice and the epididymis of non-obese diabetic (NOD) mice at the protein level to see which of these immunoregulatory proteins may be involved in lymphocyte regulation in the normal or pathological epididymis and if cytokine balance in this organ is on the cellular or humoral side. The aim of the study was to characterize the immunological microenvironment of the epididymis to explain the survival of the autoantigenic spermatozoa in this site. In the 6-week-old BALB/c or NOD mouse epididymis there were some CD18 and CD44 expressing cells in the interstitial tissue. There were no differences between these strains in the expression of the studied antigens, except that some CD4 positive cells were present in the interstitial tissue of BALB/c mice. In the cryptorchid cryptepididymis CD4, CD8, CD18, CD44, CD54 and CD106 expressing cells were occasionally present in the connective tissue surrounding the epididymal tubule. In the epididymis of the oestrogen-treated mice these antigens were not expressed. In the cryptorchid cryptepididymis the epithelial cells expressed IL-10 highly and the myoid peritubular cells IL-6. The present results suggest that the epididymal epithelial IL-10 suppressing TH0, TH1 and TH2 immune responses may be involved in the protection of autoantigenic spermatozoa from immune destruction.

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Veräjänkorva, E., Pöllänen, P., Hänninen, A., Martikainen, M., Sundström, J., & Antola, H. (2002). IL-10 is highly expressed in the cryptorchid cryptepididymal epithelium: A probable mechanism preventing immune responses against autoantigenic spermatozoa in the epididymal tubule. International Journal of Andrology, 25(3), 129–133. https://doi.org/10.1046/j.1365-2605.2002.00336.x

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