Experimental autoimmune orchitis after neonatal thymectomy in the mouse.

Experimental autoimmune orchitis (EAO) developed in (C57Bl/6Cr x A/JCr)F1 mice 3-4 months after neonatal thymectomy (Tx) without any sensitization. The age of Tx was critical for induction of EAO: Tx at day 3 (Tx-3) was effective, but Tx at day 0 or day 7 was not effective. This lesion resulted in atrophy of the testis and was characterized by disappearance of mature sperms, formation of multinuclear giant cells in seminiferous tubules and infiltration of lymphocytes in the stroma. Epididymitis was observed prior to the development of EAO. Presence of circulating autoantibody(s) against sperms (ASA) was demonstrated by indirect immunofluorescence. The acrosomal area of mature sperms, but not of immature spermatids, was strongly. The incidence of EAO and titre of ASA increased when Tx-3 mice were unilaterally vasectomized (Vx). The majority of mice with high titres of circulating ASA were sterile. Epididymitis and orchitis could be prevented in Tx-3 mice by injection of adult spleen cells on day 4. The most effective source was normal male. Spleen cells from normal female donors and day-0 orchidectomized (Orx) donors were less effective, while those of Tx-3 male and female donors failed to prevent epididymis and orchitis. The cell population in normal male spleen effective in preventing epididymitis was shown to be a T cell population (Thy 1+, Ig-) by experiments with respective antisera treatment. These results showed that sensitization with sperm autoantigen occurred in the epididymis after Tx-3, more efficiently after Tx-3 plus unilateral Vx, and that this autosensitization was prevented by a specific suppressor T cell population, which was present in normal males but absent in Tx-3 mice.