Abstract

To summarize, it may be stated that experimental allergic orchitis is an organ-specific immunologic disease that leads to damage of spermatogenesis in both testes. The pathogenesis is characterized by a complex immunologic process that is dependent on whether the antibody or the sensitized lymphocyte makes contact with testicular antigen. It is very likely that the humoral as well as cell-mediated immunologic reactions play a role and lead to the typical cellular lesions in testicular tissue.16 The blood-testis barrier seems to be the most important physiologic factor and prevents permeation of immunocompetent cells into the intratubular structures. This barrier exists between the vessels and the seminiferous tubules in the peritubular connective tissue. The hypothesis of damage to the blood-testis barrier by an unknown helping factor could be discussed, with some assumptions, as a possible model for the unilateral cryptorchid testis. It is widely reported that the environmental temperature in the abdominal cavity or the inguinal canal is 1 to 2°C higher than in the scrotum and is the reason for the damage to an undescended testis. This widely accepted hypothesis has not been proved completely. Rapaport et al. and Fernandez-Collazo et al. were able to demonstrate in a guinea pig model that brief thermic alterations lead to marked morphologic changes in both of the testes and to autoimmunoreactions as well.3. 15 These changes are similar to those created in the model of experimental allergic orchitis. According to the view of Tung et al., it is possible that a permanenthigh nonphysiologic environmental temperature makes the blood-testis barrierpermeableby immunocompetent cells. A helping factor may assist. This process may then produce an autoantibody reaction against testicular structures. Although it has not yet been possible to demonstrate antibodies against testicular structures in cases of cryptorchidism,” 9 the hypothesis of an immunopathogenic origin of pathologic changes in cryptorchid testes is supported by our own experimental studies. In the model of experimental unilateral testicular maldescent using azathioprine as an immunosuppressant, the total number of spermatogonia in the dystopic as well as in the contralateral orthotopic testis increased significantly. It is not clear why there are no cellular infiltrations in either the cryptorchid or the orthotopic testis three months after the start of the experiment. Cellular infiltrations for experimental allergic orchitis are described by various authors. The reason may be that after three months cellular infiltration may no longer be present or the mechanism may be only humoral. Our considerations regarding the immunopathogenesis of cryptorchidism attempt to explain parallels between cryptorchidism and experimental allergic orchitis. Pendingfurther study, our conclusions are hypothetical.

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