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4 results on '"María S, Theas"'

1. Immune Cell Subtypes and Their Function in the Testis

Author

Sudhanshu Bhushan, María S. Theas, Vanesa A. Guazzone, Patricia Jacobo, Ming Wang, Monika Fijak, Andreas Meinhardt, and Livia Lustig

Subjects
testis, immune privilege, macrophages, dendritic cells, T lymphocytes, mast cells, Immunologic diseases. Allergy, RC581-607
Abstract

Immunoregulation in the testis is characterized by a balance between immuno-suppression (or immune privilege) and the ability to react to infections and inflammation. In this review, we analyze the phenotypes of the various immune cell subtypes present in the testis, and how their functions change between homeostatic and inflammatory conditions. Starting with testicular macrophages, we explore how this heterogeneous population is shaped by the testicular microenvironment to ensure immune privilege. We then describe how dendritic cells exhibit a tolerogenic status under normal conditions, but proliferate, mature and then stimulate effector T-cell expansion under inflammatory conditions. Finally, we outline the two T-cell populations in the testis: CD4+/CD8+ αβ T cells and CD4+/CD8+ Foxp3+ regulatory T cells and describe the distribution and function of mast cells. All these cells help modulate innate immunity and regulate the immune response. By improving our understanding of immune cell behavior in the testis under normal and inflammatory conditions, we will be better placed to evaluate testis impairment due to immune mechanisms in affected patients.

Published
2020
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2. Pathomechanisms of Autoimmune Based Testicular Inflammation

Author

Livia Lustig, Vanesa A. Guazzone, María S. Theas, Christiane Pleuger, Patricia Jacobo, Cecilia V. Pérez, Andreas Meinhardt, and Monika Fijak

Subjects
testicular inflammation, autoimmunity, experimental autoimmune orchitis (EAO), infertility, testis immunoregulation, Immunologic diseases. Allergy, RC581-607
Abstract

Infection and inflammation of the male reproductive tract are relevant causes of infertility. Inflammatory damage occurs in the special immunosuppressive microenvironment of the testis, a hallmark termed testicular immune privilege, which allows tolerance to neo-antigens from developing germ cells appearing at puberty, long after the establishment of systemic immune tolerance. Experimental autoimmune orchitis (EAO) is a well-established rodent model of chronic testicular inflammation and organ specific autoimmunity that offers a valuable in vivo tool to investigate the pathological and molecular mechanisms leading to the breakdown of the testicular immune privilege. The disease is characterized by the infiltration of the interstitium by immune cells (mainly macrophages, dendritic cells, and T cells), formation of autoantibodies against testicular antigens, production of pro-inflammatory mediators such as NO, MCP1, TNFα, IL6, or activins and dysregulation of steroidogenesis with reduced levels of serum testosterone. EAO leads to sloughing of germ cells, atrophic seminiferous tubules and fibrotic remodeling, parameters all found similarly to changes in human biopsies from infertile patients with inflammatory infiltrates. Interestingly, testosterone supplementation during the course of EAO leads to expansion of the regulatory T cell population and inhibition of disease development. Knowledge of EAO pathogenesis aims to contribute to a better understanding of human testicular autoimmune disease as an essential prerequisite for improved diagnosis and treatment.

Published
2020
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3. Dual role of immune cells in the testis: protective or pathogenic for germ cells?

Author

Livia Lustig, Patricia Verónica Jacobo, S. Jarazo-Dietrich, Vanesa Anabella Guazzone, Cecilia Valeria Pérez, and María S. Theas

Subjects
Germinal epithelium, CIENCIAS MÉDICAS Y DE LA SALUD, germ cell apoptosis, Ciencias de la Salud, Inflammation, Review, testis, SEMINIFEROUS TUBULES, Fas ligand, purl.org/becyt/ford/3.3 [https], Immune system, immune cells, INFLAMMATION, nitric oxide, medicine, Blood–testis barrier, CD40, biology, blood-testis barrier, Cell adhesion molecule, TESTIS, CYTOKINES, Lymphokine, seminiferous tubules, cytokines, Cell biology, Otras Ciencias de la Salud, Reproductive Medicine, inflammation, IMMUNE CELLS, Immunology, biology.protein, purl.org/becyt/ford/3 [https], GERM CELL APOPTOSIS, BLOOD TESTIS BARRIER, medicine.symptom, NITRIC OXIDE
Abstract

The purpose of this review is to describe how the immune cells present in the testis interact with the germinal epithelium contributing to survival or apoptosis of germ cells (GCs). Physiologically, the immunosuppressor testicular microenvironment protects GCs from immune attack, whereas in inflammatory conditions, tolerance is disrupted and immune cells and their mediators respond to GC self antigens, inducing damage of the germinal epithelium. Considering that experimental models of autoimmune orchitis have clarified the local immune mechanisms by which protection of the testis is compromised, we described the following topics in the testis of normal and orchitic rats: (1) cell adhesion molecule expression of seminiferous tubule specialized junctions and modulation of blood-testis barrier permeability by cytokines (2) phenotypic and functional characteristics of testicular dendritic cells, macrophages, effector and regulatory T cells and mast cells and (3) effects of pro-inflammatory cytokines (TNF-α, IL-6 and FasL) and the nitric oxide-nitric oxide synthase system on GC apoptosis. Fil: Pérez, Cecilia Valeria. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina Fil: Theas, Maria Susana. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina Fil: Jacobo, Patricia Verónica. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina Fil: Jarazo Dietrich, Sabrina Soledad. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina Fil: Guazzone, Vanesa Anabella. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina Fil: Lustig, Livia. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina

Published
2013

4. Involvement of tumor necrosis factor-alpha in the pathogenesis of autoimmune orchitis in rats

Author

María O, Suescun, Claudia, Rival, María S, Theas, Ricardo S, Calandra, and Livia, Lustig

Subjects
Male, Tumor Necrosis Factor-alpha, Macrophages, Antibodies, Monoclonal, Leydig Cells, Apoptosis, Enzyme-Linked Immunosorbent Assay, Orchitis, Cell Separation, Receptors, Tumor Necrosis Factor, Autoimmune Diseases, Rats, Immunoenzyme Techniques, Rats, Sprague-Dawley, Germ Cells, Antigens, CD, Receptors, Tumor Necrosis Factor, Type I, Culture Media, Conditioned, Testis, Macrophages, Peritoneal, Animals, Cytokines, Steroids, Testosterone, Cells, Cultured
Abstract

We studied the testicular macrophages of rats with experimental autoimmune orchitis (EAO) and analyzed whether the tumor necrosis factor-alpha (TNFalpha) is involved in germ cell apoptosis and in Leydig cell steroidogenesis. The EAO was induced in adult male Sprague-Dawley rats by active immunization with testicular homogenate and adjuvants. In the experimental group, a severe orchitis was observed 80 days after the first immunization. ED1- and ED2-positive macrophages were quantified by immunohistochemistry. The TNFalpha concentration of conditioned media from testicular macrophages (TMCM) was determined by ELISA. The number of apoptotic TNF receptor 1 (TNFR1)-positive germ cells was identified by combining in situ end labeling of apoptotic DNA and immunohistochemical techniques. The effect of TNFalpha on Leydig cell testosterone production was determined by RIA. In rats with EAO, we observed a significant increase in the number of TNFalpha-positive testicular macrophages, the TNFalpha concentration in TMCM, and the number of TNFR1-positive germ cells. Sixty percent of TNFR1-positive germ cells were apoptotic. These results suggest that TNFalpha could be involved in the pathogenesis of EAO. Acting together with other local factors such as Fas-FasL, TNFalpha could trigger germ cell apoptosis. We also demonstrated that TNFalpha inhibited in vitro testosterone production in basal and hCG-stimulated Leydig cells from rats with orchitis.

Published
2003

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