Search

Your search keyword '"Desdín-Mico, Gabriela"' showing total 5 results
Start Over Author "Desdín-Mico, Gabriela"
5 results on '"Desdín-Mico, Gabriela"'

1. The role of T cells in age-related diseases

Author

Instituto de Salud Carlos III, European Commission, European Research Council, Comunidad de Madrid, Universidad Autónoma de Madrid, Fundación para la Investigación Biomédica del Hospital Universitario 12 de Octubre, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Carrasco, Elisa, Gómez de las Heras, Manuel M., Gabandé-Rodríguez, Enrique, Desdín-Mico, Gabriela, Aranda, Juan Francisco, Mittelbrunn, María, Instituto de Salud Carlos III, European Commission, European Research Council, Comunidad de Madrid, Universidad Autónoma de Madrid, Fundación para la Investigación Biomédica del Hospital Universitario 12 de Octubre, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Carrasco, Elisa, Gómez de las Heras, Manuel M., Gabandé-Rodríguez, Enrique, Desdín-Mico, Gabriela, Aranda, Juan Francisco, and Mittelbrunn, María

Abstract

Age-related T cell dysfunction can lead to failure of immune tolerance mechanisms, resulting in aberrant T cell-driven cytokine and cytotoxic responses that ultimately cause tissue damage. In this Review, we discuss the role of T cells in the onset and progression of age-associated conditions, focusing on cardiovascular disorders, metabolic dysfunction, neuroinflammation and defective tissue repair and regeneration. We present different mechanisms by which T cells contribute to inflammageing and might act as modulators of age-associated diseases, including through enhanced pro-inflammatory and cytotoxic activity, defective clearance of senescent cells or regulation of the gut microbiota. Finally, we propose that ‘resetting’ immune system tolerance or targeting pathogenic T cells could open up new therapeutic opportunities to boost resilience to age-related diseases.

Published
2022

2. Mitochondrial dysfunction defines T cell exhaustion

Author

Instituto de Salud Carlos III, European Research Council, Instituto de Investigación Hospital 12 de Octubre, Universidad Autónoma de Madrid, Soto-Heredero, Gonzalo, Desdín-Mico, Gabriela, Mittelbrunn, María, Instituto de Salud Carlos III, European Research Council, Instituto de Investigación Hospital 12 de Octubre, Universidad Autónoma de Madrid, Soto-Heredero, Gonzalo, Desdín-Mico, Gabriela, and Mittelbrunn, María

Abstract

When T cells are exposed to continuous antigen stimulation, they become exhausted. Here, we preview findings from Scharping et al., who have illuminated the molecular mechanism by which the persistent antigen stimulation and severe hypoxic conditions in the intratumoral environment drive T cell exhaustion, losing their cytotoxic function and anticancer effects.When T cells are exposed to continuous antigen stimulation, they become exhausted. Here, we preview findings from Scharping et al. (2021), who have illuminated the molecular mechanism by which the persistent antigen stimulation and severe hypoxic conditions in the intratumoral environment drive T cell exhaustion, losing their cytotoxic function and anticancer effects.

Published
2021

3. Extracellular Tuning of Mitochondrial Respiration Leads to Aortic Aneurysm

Author

Instituto de Salud Carlos III, European Commission, Comunidad de Madrid, Instituto de Investigación Hospital 12 de Octubre, Oller, Jorge, Gabandé-Roldríguez, Enrique, Ruíz-Rodríguez, María J., Desdín-Mico, Gabriela, Aranda, Juan Francisco, Rodriguez-Díez, Raquel, Ballesteros-Martínez, Constanza, Blanco, Eva M., Roldan-Montero, Raquel, Acuña, Pedro, Forteza Gil, Alberto, Martín-López, Carlos E., Nistal, J. Francisco, Lino Cardenas, Christian L, Lindsay, Mark Evan, Martín-Ventura, Jose Luis, Briones, Ana M., Miguel Redondo, Juan, Mittelbrunn, María, Instituto de Salud Carlos III, European Commission, Comunidad de Madrid, Instituto de Investigación Hospital 12 de Octubre, Oller, Jorge, Gabandé-Roldríguez, Enrique, Ruíz-Rodríguez, María J., Desdín-Mico, Gabriela, Aranda, Juan Francisco, Rodriguez-Díez, Raquel, Ballesteros-Martínez, Constanza, Blanco, Eva M., Roldan-Montero, Raquel, Acuña, Pedro, Forteza Gil, Alberto, Martín-López, Carlos E., Nistal, J. Francisco, Lino Cardenas, Christian L, Lindsay, Mark Evan, Martín-Ventura, Jose Luis, Briones, Ana M., Miguel Redondo, Juan, and Mittelbrunn, María

Abstract

Marfan syndrome (MFS) is an autosomal dominant disorder of the connective tissue caused by mutations in the FBN1 (fibrillin-1) gene encoding a large glycoprotein in the extracellular matrix called fibrillin-1. The major complication of this connective disorder is the risk to develop thoracic aortic aneurysm. To date, no effective pharmacologic therapies have been identified for the management of thoracic aortic disease and the only options capable of preventing aneurysm rupture are endovascular repair or open surgery. Here, we have studied the role of mitochondrial dysfunction in the progression of thoracic aortic aneurysm and mitochondrial boosting strategies as a potential treatment to managing aortic aneurysms.

Published
2021

4. T cells with dysfunctional mitochondria induce multimorbidity and premature senescence

Author

Instituto de Salud Carlos III, European Commission, European Research Council, Comunidad de Madrid, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Desdín-Mico, Gabriela, Soto-Heredero, Gonzalo, Aranda, Juan Francisco, Oller, Jorge, Carrasco, Elisa, Gabandé-Rodríguez, Enrique, Blanco, Eva M., Alfranca, Arantzazu, Cussó, Lorena, Desco, Manuel, Ibañez, Borja, Gortazar, Arancha R., Fernández-Marcos, Pablo, Navarro, María N., Hernaez, Bruno, Alcamí, Antonio, Baixauli, Francesc, Mittelbrunn, María, Instituto de Salud Carlos III, European Commission, European Research Council, Comunidad de Madrid, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Desdín-Mico, Gabriela, Soto-Heredero, Gonzalo, Aranda, Juan Francisco, Oller, Jorge, Carrasco, Elisa, Gabandé-Rodríguez, Enrique, Blanco, Eva M., Alfranca, Arantzazu, Cussó, Lorena, Desco, Manuel, Ibañez, Borja, Gortazar, Arancha R., Fernández-Marcos, Pablo, Navarro, María N., Hernaez, Bruno, Alcamí, Antonio, Baixauli, Francesc, and Mittelbrunn, María

Abstract

The effect of immunometabolism on age-associated diseases remains uncertain. In this work, we show that T cells with dysfunctional mitochondria owing to mitochondrial transcription factor A (TFAM) deficiency act as accelerators of senescence. In mice, these cells instigate multiple aging-related features, including metabolic, cognitive, physical, and cardiovascular alterations, which together result in premature death. T cell metabolic failure induces the accumulation of circulating cytokines, which resembles the chronic inflammation that is characteristic of aging (“inflammaging”). This cytokine storm itself acts as a systemic inducer of senescence. Blocking tumor necrosis factor-a signaling or preventing senescence with nicotinamide adenine dinucleotide precursors partially rescues premature aging in mice with Tfam-deficient T cells. Thus, T cells can regulate organismal fitness and life span, which highlights the importance of tight immunometabolic control in both aging and the onset of age-associated diseases.

Published
2020

Catalog

Books, media, physical & digital resources
See catalog results