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Experimental allergic orchitis in mice. VII.Preliminary characterization of the aspermatogenic autoantigensresponsible for eliciting actively and passively induced disease.
Links Experimental allergic orchitis in mice. VII. Preliminary characterization of the aspermatogenic autoantigens responsible for eliciting actively and passively induced disease. Teuscher C, Meeker ND, Livingstone KD, Sudweeks JD, Griffith JS, Wardell BB, Hickey WFJ Reprod Immunol. 1994 May;26(3):233-49. Links Experimental allergic orchitis in mice. VII. Preliminary characterization of the aspermatogenic autoantigens responsible for eliciting actively and passively induced disease. Teuscher C, Meeker ND, Livingstone KD, Sudweeks JD, Griffith JS, Wardell BB, Hickey WF. Department of Microbiology, Brigham Young University, Provo, UT 84602. Experimental allergic orchitis (EAO) can be induced actively and passively 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, naive recipients. The distribution of inflammatory lesions seen in active and passive EAO are markedly different. In active EAO maximal disease is observed in the seminiferous tubules, whereas in passive EAO lesions occur primarily in the straight tubules, rete testis, and ductus efferentes. These observations suggest that different immunopathogenic mechanisms and/or aspermatogenic autoantigens may be responsible for the distinct histopathologic profiles. Two murine testis-specific aspermatogenic autoantigens (mAP1 and mAP2) were partially purified from MT acetone powder by extraction in 7-M urea under reducing conditions, gel filtration, ion-exchange chromatography, and preparative isoelectric focusing from pH 3 to 10. In gel filtration on Sephacryl S-400 in 7-M urea, mAP1 is confined to the V0 peak, while mAP2 is in the major included 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 micrograms (dry wt). Dose-response bioassays for active and passive EAO revealed that mAP1 preferentially elicits active disease, whereas 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 immunopathologic responses elicited by separate aspermatogenic autoantigens. PMID: 7990075 [PubMed - indexed for MEDLINE] Related Links Distribution of histopathology and Ia positive cells in actively induced and passively transferred experimental autoimmune orchitis. [J Immunol. 1987] PMID: 3492532 Experimental allergic orchitis in mice: IV. Preliminary characterization of the major murine testis specific aspermatogenic autoantigen(s). [J Reprod Immunol. 1987] PMID: 3501013 Experimental allergic orchitis in mice. V. Resistance to actively induced disease in BALB/cJ substrain mice is mediated by CD4+ T cells. [Immunogenetics. 1990] PMID: 1973683 Actively-induced experimental allergic orchitis (EAO) in Lewis/NCR rats: sequential histo- and immunopathologic analysis. [Autoimmunity. 1989] PMID: 2491624 Role of testicular autoantigens and influence of lymphokines in testicular autoimmune disease. [J Reprod Immunol. 1990] PMID: 2213733 See all Related Articles... Display Summary Brief Abstract AbstractPlus Citation MEDLINE XML UI List LinkOut ASN.1 Related Articles Cited Articles Cited in Books CancerChrom Links Domain Links 3D Domain Links GEO DataSet Links Gene Links Gene (GeneRIF) Links Genome Links Project Links GENSAT Links GEO Profile Links HomoloGene Links Nucleotide Links Nucleotide (RefSeq) Links OMIA Links OMIM (calculated) Links OMIM (cited) Links BioAssay Links Compound Links Compound via MeSH Substance Links Substance via MeSH PMC Links Cited in PMC PopSet Links Probe Links Protein Links Protein (RefSeq) Links SNP Links Structure Links Taxonomy via GenBank UniGene Links UniSTS Links Show 5 10 20 50 100 200 500 Sort by Pub Date First Author Last Author Journal Send to Text File Printer Clipboard E-mail Order .
Department of Microbiology, Brigham Young University, Provo, UT 84602.
Experimental allergic orchitis (EAO) can be induced actively and passively 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, naive recipients. The distribution of inflammatory lesions seen in active and passive EAO are markedly different. In active EAO maximal disease is observed in the seminiferous tubules, whereas in passive EAO lesions occur primarily in the straight tubules, rete testis, and ductus efferentes. These observations suggest that different immunopathogenic mechanisms and/or aspermatogenic autoantigens may be responsible for the distinct histopathologic profiles. Two murine testis-specific aspermatogenic autoantigens (mAP1 and mAP2) were partially purified from MT acetone powder by extraction in 7-M urea under reducing conditions, gel filtration, ion-exchange chromatography, and preparative isoelectric focusing from pH 3 to 10. In gel filtration on Sephacryl S-400 in 7-M urea, mAP1 is confined to the V0 peak, while mAP2 is in the major included 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 micrograms (dry wt). Dose-response bioassays for active and passive EAO revealed that mAP1 preferentially elicits active disease, whereas 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 immunopathologic responses elicited by separate aspermatogenic autoantigens.
This abstract is being posted for educational purposes, as well as for comment and criticism, by the visitors to the Epididymitis Foundation website (EpididymitisFoundation.org). This abstract is representative of a larger article that is indexed on Medline.
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