AIMS: To provide a marker for immature and dysgenetic Sertoli cells which allows easy identification in patients in which Sertoli cell maturation does not take place properly, such as those consulting for cryptorchidism, testicular tumours and infertility. METHODS AND RESULTS: We performed immunohistochemistry against inhibin-α subunit and the endoplasmic reticulum marker Grp78 in normal human testes from fetal life to adulthood, and in several testicular lesions where Sertoli cell maturation is abnormal. We describe a pattern of inhibin immunostain (inhibin bodies of 2-9 μm in diameter at the Sertoli cells cytoplasm apical pole) in immature and dysgenetic Sertoli cells that facilitates their identification. Inhibin bodies were found in tubules with either no germ cells or only spermatogonia or carcinoma in situ (CIS) and seminoma cells, but not in tubules containing more advanced germ cells. CONCLUSIONS: Our data provide a new marker of immature and dysgenetic Sertoli cells. In addition, our data suggest that inhibin bodies represent a slower transit of inhibin through the endoplasmic reticulum, as inhibin bodies were associated with Grp78.
AIMS: To provide a marker for immature and dysgenetic Sertoli cells which allows easy identification in patients in which Sertoli cell maturation does not take place properly, such as those consulting for cryptorchidism, testicular tumours and infertility. METHODS AND RESULTS: We performed immunohistochemistry against inhibin-α subunit and the endoplasmic reticulum marker Grp78 in normal human testes from fetal life to adulthood, and in several testicular lesions where Sertoli cell maturation is abnormal. We describe a pattern of inhibin immunostain (inhibin bodies of 2-9 μm in diameter at the Sertoli cells cytoplasm apical pole) in immature and dysgenetic Sertoli cells that facilitates their identification. Inhibin bodies were found in tubules with either no germ cells or only spermatogonia or carcinoma in situ (CIS) and seminoma cells, but not in tubules containing more advanced germ cells. CONCLUSIONS: Our data provide a new marker of immature and dysgenetic Sertoli cells. In addition, our data suggest that inhibin bodies represent a slower transit of inhibin through the endoplasmic reticulum, as inhibin bodies were associated with Grp78.