EXPERIMENTAL ALLERGIC ORCHITIS IN MICE .7. PRELIMINARY CHARACTERIZATION OF THE ASPERMATOGENIC AUTOANTIGENS RESPONSIBLE FOR ELICITING ACTIVELY AND PASSIVELY INDUCED DISEASE

Experimental allergic orchitis (EAO) can be induced actively and passi vely in mice by either immunization with mouse testicular homogenate ( MTH) in conjunction with the appropriate adjuvants or by transferring CD4(+) T cells isolated from sensitized donors into non-immunized, nat ive recipients. The distribution of inflammatory lesions seen in activ e and passive EAO are markedly different. In active EAO maximal diseas e is observed in the seminiferous tubules, whereas in passive EAO lesi ons occur primarily in the straight tubules, rete testis, and ductus e fferentes. These observations suggest that different immunopathogenic mechanisms and/or aspermatogenic autoantigens may be responsible for t he distinct histopathologic profiles. Two murine testis-specific asper matogenic autoantigens (mAP1 and mAP2) were partially purified from MT acetone powder by extraction in 7-M urea under reducing conditions, g el filtration, ion-exchange chromatography, and preparative isoelectri c focusing from pH 3 to 10. In gel filtration on Sephacryl S-400 in 7- M urea, mAP1 is confined to the V-0 peak while mAP2 is in the major in cluded peak. mAP1 has an isoelectric point of 4.4-4.9, is sensitive to both pronase and DNase but not RNase, and is active at a minimal dose of 250-500 mu g (dry wt). Dose-response bioassays for active and pass ive EAO revealed that mAP1 preferentially elicits active disease, wher eas mAP2 is most effective at eliciting passive disease. These results support the concept that the different histopathologic profiles seen in active and passive EAO are, in part, the result of different immuno pathologic responses elicited by separate aspermatogenic autoantigens.