Distribution of Histopathology and Ia Positive Cells in Actively Induced and Passively Transferred Experimental Autoimmune Orchitisa

Tung, Kenneth S. K.; Yule, Terecita D.; Mahi‐Brown, Cherrie A.; Listrom, Margaret B.

doi:10.1111/j.1749-6632.1987.tb25096.x

Cited by 36 publications

(68 citation statements)

References 4 publications

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“…Tung). The score was determined by the summation of testicular and epididymal inflammation, percentage of abnormal spermatogenesis, and epididymal sperm loss (24). Inflammation was graded from 0 to 4 (0 = none, 1 = very focal, and 4 = extremely severe with necrosis).…”

Section: Methodsmentioning

confidence: 99%

“…Testis homogenate was prepared and EAO was induced as previously described (24). Testis homogenate at 10 mg dry weight in CFA (4.5 mg/ml of Mycobacterium tuberculosis H37Ra, DIFCO) was injected in 1 hind footpad and 2 s.c. sites.…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, loss of tolerance rather than loss of sequestration is the likely cause of autoimmune Because the Sertoli cell barrier effectively blocks Abs and lymphoid cells from entering the seminiferous tubules (22)(23)(24), the barrier is presumed to also prevent MGCA from entering the interstitial space to reach the immune cells (19,(25)(26)(27). Accordingly, local antigen nonspecific mechanisms are deemed sufficient to control tissue barrier integrity and excessive testis inflammation in autoimmunity, trauma, or infection (19,25,27).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Egress of sperm autoantigen from seminiferous tubules maintains systemic tolerance

Tung

Harakal

Qiao

et al. 2017

Journal of Clinical Investigation

103

104

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Egress of sperm autoantigen from seminiferous tubules maintains systemic tolerance

Tung

Harakal

Qiao

et al. 2017

Journal of Clinical Investigation

103

104

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“…Previous investigations have suggested that the distribution of autoimmune inflammation can be influenced by a number of factors, including the presence of appropriate T cell subsets (4), activated macrophages (5), and proinflammatory cytokines (6,7). It may also be affected by the location of MHC class II expression (8,9), tissue barrier that affects accessibility of T cells to the target Ag (9 -11), and changes in the target organ (12,13). In the present study, we provide evidence that autoantibody can target T cell injury to the ovarian follicles and eliminates the functional unit of the ovary.…”

Section: Retargeting T Cell-mediatedmentioning

confidence: 99%

Retargeting T Cell-Mediated Inflammation: A New Perspective on Autoantibody Action

Lou

Park

Agersborg

et al. 2000

The Journal of Immunology

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To understand the pathogenesis of organ-specific autoimmune disease requires an appreciation of how the T cell-mediated inflammation is targeted, and how the organ function is compromised. In this study, autoantibody was documented to influence both of these parameters by modulating the distribution of T cell-mediated inflammation. The murine autoimmune ovarian disease is induced by immunization with the ZP3330–342 peptide of the ovarian zona pellucida 3 glycoprotein, ZP3. Passively transferred or actively induced Ab to ZP3335–342 bound to the zona pellucida in the functional and degenerative ovarian follicles, and the ovaries remained histologically normal. Transfer of ZP3330–342 peptide-specific T cells targeted the degenerative follicles and spared the functional follicles, and the resultant interstitial oophoritis was associated with unimpaired ovarian function. Unexpectedly, the coexistence of ZP3330–342 peptide-specific T cells and zona-bound autoantibody led to a dramatic translocation of the ovarian inflammation to the growing and mature ovarian follicles, with destruction of the ovarian functional unit. Ab retargeted both Th1-induced mononuclear inflammation and Th2-induced eosinophilic inflammation, and retargeting was induced by murine and rat polyclonal Abs to multiple distinct native B cell determinants of the zona pellucida. Therefore, by reacting with the native determinants in tissue Ag, Ab alters the distribution of T cell-mediated inflammation, and results in destruction of the functional units of the target organ. We propose that this is a clinically important and previously unappreciated element of Ab action in autoimmune disease.

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“…In most EAO models, epididymitis occurs prior to orchitis, and the inflammatory lesions of the epididymides usually become more severe than those in the testes (Sato et al 1981, Taguchi & Nishizuka 1981, Tung et al 1987, Roper et al 1998. Taguchi & Nishizuka (1981) were the first to investigate the effects of Vx on EAO in mice.…”

Section: Introductionmentioning

confidence: 99%

Caput epididymitis but not orchitis was induced by vasectomy in a murine model of experimental autoimmune orchitis

Terayama²,

Naito³

et al. 2008

Reproduction

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Immunization of mice with viable syngeneic testicular germ cells (TGC) alone can induce autoimmune responses against autoantigens of both round and elongating spermatids, resulting in the development of experimental autoimmune orchitis (EAO). Histological lesions in this EAO model without an adjuvant are characterized by lymphocytic infiltration into the testes, spermatogenic disturbance, and a complete lack of epididymitis. In this study, we investigated the effects of vasectomy (Vx) on TGC-induced EAO expecting that Vx augments the severity of testicular inflammation in A/J mice. The results showed that mice receiving Vx alone exhibited no significant inflammatory cell response in either the testes or epididymides, and mice receiving shamVxCTGC immunization had EAO with no epididymitis. In sharp contrast, no EAO was found in the testes of any mice receiving VxCTGC immunization. Instead, caput epididymitis involving CD4CT cells, CD8CT cells, B cells, and macrophages were induced in them with striking elevation of the tissue levels of both IL6 and IL10 mRNA. Furthermore, serum autoantibodies induced by shamVxCTGC immunization were reactive with both round (immature) and elongating (mature) spermatids; however, those induced by VxCTGC immunization were specific to acrosomes of mature spermatids and spermatozoa. These unexpected results indicate that Vx may induce the mode by which autoreactive lymphocytes gain access to TGC autoantigens in the epididymides, leading to autoimmune responses against the autoantigens of mature rather than immature spermatids. Reproduction (2008) 135 859-866

show abstract

Distribution of Histopathology and Ia Positive Cells in Actively Induced and Passively Transferred Experimental Autoimmune Orchitisa

Cited by 36 publications

References 4 publications

Egress of sperm autoantigen from seminiferous tubules maintains systemic tolerance

Egress of sperm autoantigen from seminiferous tubules maintains systemic tolerance

Retargeting T Cell-Mediated Inflammation: A New Perspective on Autoantibody Action

Caput epididymitis but not orchitis was induced by vasectomy in a murine model of experimental autoimmune orchitis

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