Inflammation and Spermatogenesis

Abstract

The testis is an immunologically privileged site with a unique immunosuppressor microenvironment able to tolerate haploid germ cell antigens that appear at puberty and to easily accept tissue grafts. However, this immunosuppressed microenvironment does not prevent the testis from developing inflammatory and immune reactions in response to different stressors such as pathogens or tissue damage. Under inflammatory conditions spermatocytes and spermatids are the main target of immunological attack; these cells die by apoptosis through external and mitochondrial pathways, whereas basal germ cells are protected from death by overexpressing Bcl-260. Diagnosis of human autoimmune orchitis associated with subfertility or infertility, a chronic inflammatory pathology, is possible only by histopathological evaluation of testis biopsy, an invasive procedure. In pathologies like orchitis and spermatogenic arrest, regeneration of spermatogenesis seems to be possible since spermatogonia remain within the seminiferous tubules despite the loss of postmeiotic germ cells.