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Evidence for active immunological regulation inprevention of testicular autoimmune disease independent of theblood-testis barrier.
Links Evidence for active immunological regulation in prevention of testicular autoimmune disease independent of the blood-testis barrier. Mahi-Brown CA, Yule TD, Tung KSAm J Reprod Immunol Microbiol. 1988 Apr;16(4):165-70. Links Evidence for active immunological regulation in prevention of testicular autoimmune disease independent of the blood-testis barrier. Mahi-Brown CA, Yule TD, Tung KS. University of New Mexico, School of Medicine, Department of Pathology, Albuquerque 87131. It has long been considered that autoimmune disease of the testis is prevented by sequestration of testis-specific autoantigens on germ cells behind the blood-testis (BT) barrier. However, we now have evidence that not all such antigens are sequestered. Some appear to reside on germ cells in the basal compartment of the seminiferous tubule where they are accessible to antibodies and to circulating activated T cells. Mice immunized with syngeneic testis homogenate are found to have immunoglobulin G (IgG) bound to cells in the basal compartment before onset of orchitis. This IgG is absorbed from circulation by the testis and, therefore, found only in the serum of mice orchiectomized before immunization. When the IgG is eluted from the testis, it is found to react preferentially with testicular cells enriched in preleptotene spermatocytes. T cells from mice immunized with testis can be transferred to naive syngeneic mice where they infiltrate the testis to cause orchitis. This implies that the BT barrier does not need to be breached directly for specific T cells to have access to testicular autoantigens on antigen presenting cells. Thus, active systemic and/or local immunoregulatory mechanisms must operate to prevent testicular autoimmune disease. These mechanisms may operate at the level of suppressor T cells, nonspecific suppression in the local environment of the testis, antigen presentation in the testis, or lymphocyte trafficking in the testis. These mechanisms probably operate only on the afferent limb of the immune response since they are overridden and orchitis occurs once testis-specific activated T cells are generated. PMID: 3048131 [PubMed - indexed for MEDLINE] Related Links Role of testicular autoantigens and influence of lymphokines in testicular autoimmune disease. [J Reprod Immunol. 1990] PMID: 2213733 Autoantigenic germ cells exist outside the blood testis barrier. [J Immunol. 1988] PMID: 3397538 Experimental autoimmune orchitis induced by testis and sperm antigen-specific T cell clones: an important pathogenic cytokine is tumor necrosis factor. [Endocrinology. 1993] PMID: 8103448 Distribution of histopathology and Ia positive cells in actively induced and passively transferred experimental autoimmune orchitis. [J Immunol. 1987] PMID: 3492532 Macrophages activated by Listeria monocytogenes induce organ-specific autoimmunity. [Immunology. 1997] PMID: 9415037 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 .
University of New Mexico, School of Medicine, Department of Pathology, Albuquerque 87131.
It has long been considered that autoimmune disease of the testis is prevented by sequestration of testis-specific autoantigens on germ cells behind the blood-testis (BT) barrier. However, we now have evidence that not all such antigens are sequestered. Some appear to reside on germ cells in the basal compartment of the seminiferous tubule where they are accessible to antibodies and to circulating activated T cells. Mice immunized with syngeneic testis homogenate are found to have immunoglobulin G (IgG) bound to cells in the basal compartment before onset of orchitis. This IgG is absorbed from circulation by the testis and, therefore, found only in the serum of mice orchiectomized before immunization. When the IgG is eluted from the testis, it is found to react preferentially with testicular cells enriched in preleptotene spermatocytes. T cells from mice immunized with testis can be transferred to naive syngeneic mice where they infiltrate the testis to cause orchitis. This implies that the BT barrier does not need to be breached directly for specific T cells to have access to testicular autoantigens on antigen presenting cells. Thus, active systemic and/or local immunoregulatory mechanisms must operate to prevent testicular autoimmune disease. These mechanisms may operate at the level of suppressor T cells, nonspecific suppression in the local environment of the testis, antigen presentation in the testis, or lymphocyte trafficking in the testis. These mechanisms probably operate only on the afferent limb of the immune response since they are overridden and orchitis occurs once testis-specific activated T cells are generated.
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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