Adoptive transfer of murine autoimmune orchitis to naive recipients with immune lymphocytes

A protocol was developed for reproducibly transferring experimental autoimmune orchitis (EAO) to naive recipient mice. Cell donors were (C57BL/6 × A/J)F1 mice immunized about 14 days earlier with mouse testicular homogenate with Freund's adjuvant and an extract of Bordetella pertussis. Lymphocy...

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Veröffentlicht in:Cellular immunology 1987-05, Vol.106 (2), p.408-419
Hauptverfasser: Mahi-Brown, Cherrie A., Yule, Terecita D., Tung, Kenneth S.K.
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Sprache:eng
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Zusammenfassung:A protocol was developed for reproducibly transferring experimental autoimmune orchitis (EAO) to naive recipient mice. Cell donors were (C57BL/6 × A/J)F1 mice immunized about 14 days earlier with mouse testicular homogenate with Freund's adjuvant and an extract of Bordetella pertussis. Lymphocytes from lymph nodes and spleens were equally capable of transferring disease. As few as 5 × 10 6 cells were able to transfer EAO, which began on Day 5–7 after transfer. Infiltrate of lymphocytes and macrophages in the region of the rete testis and straight tubules was the most reproducible early lesion, suggesting that this is the initial site of T cell-antigen interaction. It was not necessary to use both Mycobacteria and B. pertussis adjuvants in donor immunization to achieve transfer of EAO. Disease transfer was antigen specific since only cells from donors immunized with TH could transfer disease. In vitro stimulation of the cells with testicular antigens and/or concanavalin A was a prerequisite to successful transfer of EAO, which was dependent on the presence of L3T4 + T cells since depletion of these cells greatly diminished EAO in recipients and the lymphocyte proliferation response to testicular antigens. Disease did not depend on an antibody response by the recipients. The results imply that effector cells, once generated by immunization and fully activated or selected by in vitro stimulation, can home to specific locations in the testis, locate relevant autoantigens, and cause disease.
ISSN:0008-8749
1090-2163
DOI:10.1016/0008-8749(87)90183-3