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

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

doi:10.1016/0008-8749(87)90183-3

Cited by 79 publications

(38 citation statements)

References 35 publications

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“…Yet, these new autoantigens are tolerated by the testis despite the fact that their immunogenicity is preserved; indeed, they induce strong autoimmune reactions when injected elsewhere in the body [1][2][3], and this orchitis can be transferred to nonimmunized recipients via activated lymphocytes [4]. The blood-testis barrier, formed by Sertoli cells in the seminiferous epithelium, does not entirely segregate differentiating germ cells from the systemic circulation [5], and it has been demonstrated to be incomplete in some areas (for review see [6]).…”

Section: Introductionmentioning

confidence: 99%

Mouse Sertoli Cells Display Phenotypical and Functional Traits of Antigen-Presenting Cells in Response to Interferon Gamma

Secco

Riccioli

Padula

et al. 2008

Biology of Reproduction

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The testis is regarded as an immunologically privileged site because it tolerates either autoantigenic germ cells or allografts. Because the blood testis barrier represents an incomplete immunological barrier, we have explored whether Sertoli cells, the somatic cells of the seminiferous epithelium, might play an active role in immune evasion. We report data indicating that B7-H1(officially known as CD274)-mediated co-inhibition, an immunomodulatory mechanism based on cell-cell interaction, can be activated in Sertoli cell-lymphocyte cocultures. We have found that, in response to interferon gamma (IFNG), mouse Sertoli cells strongly up-regulate the negative co-stimulatory ligand B7-H1 but remain devoid of positive co-stimulatory molecules. Blockade of B7-H1 on the Sertoli cell surface resulted in enhanced proliferation of CD8(+) T cells cocultured with Sertoli cells. Moreover, IFNG-stimulated Sertoli cells were found to express, concurrent with B7-H1, MHC class II. Therefore, we have hypothesized that Sertoli cells could function as nonprofessional tolerogenic antigen-presenting cells by inducing enrichment in regulatory T cells (Tregs) in a mixed T lymphocyte population. Interestingly, we found that coculturing T cells with Sertoli cells can indeed induce an increase in CD4(+)CD25(+)(officially known as IL2RA)FOXP3(+) Tregs and a decrease in CD4(+)CD25(-) T cells, suggesting Sertoli cell-mediated Treg conversion; this process was found to be B7-H1-independent. Altogether these data show that Sertoli cells are potentially capable of down-regulating the local immune response, on one hand by directly inhibiting CD8(+) T cell proliferation through B7-H1 and, on the other hand, by inducing an increase in Tregs that might suppress other bystander T cells.

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Section: Introductionmentioning

confidence: 99%

Mouse Sertoli Cells Display Phenotypical and Functional Traits of Antigen-Presenting Cells in Response to Interferon Gamma

Secco

Riccioli

Padula

et al. 2008

Biology of Reproduction

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“…Antigenic challenge or activated lymphocyte cell transfer can induce autoimmune disease against most immune privileged sites including the testes [53,54], cornea [55], and pregnant uterus [56]. Any putative hair follicle IP may also similarly be broken by activating the immune system against hair follicle autoantigens.…”

Section: Immune Privilege Collapse In Alopecia Areatamentioning

confidence: 99%

The role of lymphocytes in the development and treatment of alopecia areata

Guo

Cheng

Shapiro

et al. 2015

Expert Review of Clinical Immunology

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SummaryAlopecia areata (AA) development is associated with both innate and adaptive immune cell activation, migration to peri-and intra-follicular regions, and hair follicle disruption. Both CD4+ and CD8+ lymphocytes are abundant in AA lesions; however, CD8+ cytotoxic T lymphocytes are more likely to enter inside hair follicles, circumstantially suggesting that they have a significant role to play in AA development. Several rodent models recapitulate important features of the human autoimmune disease and demonstrate that CD8+ cytotoxic T lymphocytes are fundamentally required for AA induction and perpetuation. However, the initiating events, the selfantigens involved, and the molecular signaling pathways, all need further exploration. Studying CD8+ cytotoxic T lymphocytes and their fate decisions in AA development may reveal new and improved treatment approaches.

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“…These results (ability to transfer increased susceptibility to i.t. M. faeni can be depressed or ablated by anti-Thy1.2, anti-Ia or anti-CD4 antibody, but not anti-CD8, antibody at the onset of culture) are similar to those found in EAE [14][15][16][17], experimental autoimmune orchitis [18] and experimental autoimmune thyroiditis [19].…”

Section: Discussionmentioning

confidence: 71%

Experimental hypersensitivity pneumonitis: cellular requirements

Schuyler

Gott

Edwards

1996

Clinical and Experimental Immunology

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SUMMARYWe previously demonstrated that Thy1.2 + , CD4 + , Ia ÿ T cells are responsible for transfer of murine adoptive experimental hypersensitivity pneumonitis (adoptive EHP). To characterize the culture conditions necessary for development of these cells, we depleted cell cultures of Thy1.2 + , CD4 + , CD8 + , or Ia + cells using MoAbs and complement or magnetic beads, prior to culture of sensitized C3H/HeJ murine spleen cells (SC) with Micropolyspora faeni. After culture, cells were transferred to recipients which were later challenged intratracheally with M. faeni. The extent of pulmonary inflammatory changes in these animals was determined 4 days after intratracheal (i.t.) challenge with M. faeni. Cultured M. faeni-sensitized SC which had been treated before culture with media, complement only, anti-CD8 plus complement or magnetic beads alone could transfer EHP to naive animals. SC treated with anti-Thy1.2 or anti-CD4 plus complement could not transfer EHP. Treatment of SC with anti-Ia k plus magnetic beads diminished the ability of cultured cells to transfer EHP. We conclude that the ability to produce cells able to adoptively transfer EHP is dependent on the presence of Thy1.2 + , CD4 + and Ia + cells, but not CD8 + cells, at the onset of culture.

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

Cited by 79 publications

References 35 publications

Mouse Sertoli Cells Display Phenotypical and Functional Traits of Antigen-Presenting Cells in Response to Interferon Gamma

Mouse Sertoli Cells Display Phenotypical and Functional Traits of Antigen-Presenting Cells in Response to Interferon Gamma

The role of lymphocytes in the development and treatment of alopecia areata

Experimental hypersensitivity pneumonitis: cellular requirements

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