Browsing by Author "Riedel, C.A."

Now showing 1 - 3 of 3
  • No Thumbnail Available
    Item
    Gestational hypothyroidism increases the severity of experimental autoimmune encephalomyelitis in adult offspring
    (2013) Albornoz, E.A.; Carreño, L.J.; Cortes, C.M.; Gonzalez, P.A.; Cisternas, P.A.; Cautivo, K.M.; Catalán, T.P.; Opazo, M.C.; Eugenin, E.A.; Berman, J.W.; Bueno Ramirez, Susan Marcela; Kalergis, Alexis M.; Riedel, C.A.
    Background: Maternal thyroid hormones play a fundamental role in appropriate fetal development during gestation. Offspring that have been gestated under maternal hypothyroidism suffer cognitive impairment. Thyroid hormone deficiency during gestation can significantly impact the central nervous system by altering the migration, differentiation, and function of neurons, oligodendrocytes, and astrocytes. Given that gestational hypothyroidism alters the immune cell ratio in offspring, it is possible that this condition could result in higher sensitivity for the development of autoimmune diseases. Methods: Adult mice gestated under hypothyroidism were induced with experimental autoimmune encephalomyelitis (EAE). Twenty-one days after EAE induction, the disease score, myelin content, immune cell infiltration, and oligodendrocyte death were evaluated. Results: We observed that mice gestated under hypothyroidism showed higher EAE scores after disease induction during adulthood compared to mice gestated in euthyroidism. In addition, spinal cord sections of mice gestated under hypothyroidism that suffered EAE in adulthood showed higher demyelination, CD4+ and CD8+ infiltration, and increased oligodendrocyte death. Conclusions: These results show for the first time that a deficiency in maternal thyroid hormones during gestation can influence the outcome of a central nervous system inflammatory disease, such as EAE, in their offspring. These data strongly support evaluating thyroid hormones in pregnant women and treating hypothyroidism during pregnancy to prevent increased susceptibility to inflammatory diseases in the central nervous system of offspring. © Copyright 2013, Mary Ann Liebert, Inc. 2013.
  • Thumbnail Image
    Item
    Intestinal Microbiota Influences Non-intestinal Related Autoimmune Diseases
    (2018) Opazo, M.C.; Ortega-Rocha, E.M.; Coronado Arrázola, Irenice; Bonifaz, L.C.; Boudin, H.; Neulist, M.; Bueno Ramírez, Susan; Kalergis Parra, Alexis Mikes; Riedel, C.A.
  • Thumbnail Image
    Item
    Modulation of tumor immunity by soluble and membrane-bound molecules at the immunological synapse
    (2013) González, P.A.; Carreño, L.J.; Céspedes, P.F.; Bueno, S.M.; Riedel, C.A.; Kalergis, A.M.
    To circumvent pathology caused by infectious microbes and tumor growth, the host immune system must constantly clear harmful microorganisms and potentially malignant transformed cells. This task is accomplished in part by T-cells, which can directly kill infected or tumorigenic cells. A crucial event determining the recognition and elimination of detrimental cells is antigen recognition by the T cell receptor (TCR) expressed on the surface of T cells. Upon binding of the TCR to cognate peptide-MHC complexes presented on the surface of antigen presenting cells (APCs), a specialized supramolecular structure known as the immunological synapse (IS) assembles at the T cell-APC interface. Such a structure involves massive redistribution of membrane proteins, including TCR/pMHC complexes, modulatory receptor pairs, and adhesion molecules. Furthermore, assembly of the immunological synapse leads to intracellular events that modulate and define the magnitude and characteristics of the T cell response. Here, we discuss recent literature on the regulation and assembly of IS and the mechanisms evolved by tumors to modulate its function to escape T cell cytotoxicity, as well as novel strategies targeting the IS for therapy.