Publications

CD4 T cell therapy counteracts inflammaging and senescence by preserving gut barrier integrity

Gómez de Las Heras MM, Carrasco E, Pérez-Manrique M, Inohara N, Delgado-Pulido S, Fernández-Almeida Á, Gálvez-Castaño MI, Francos-Quijorna I, Simó C, García-Cañas V, Escrig-Larena JI, Aranda JF, Soto-Heredero G, Gabandé-Rodríguez E, Blanco EM, Días-Almeida J, Núñez G, Mittelbrunn M.

Sci Immunol. 2025 Aug;10(110):eadv0985;

  • PMID: 40749035 
  • DOI: 10.1126/sciimmunol.adv0985

Healthy aging relies on a symbiotic host-microbiota relationship. The age-associated decline of the immune system can pose a threat to this delicate equilibrium. In this work, we investigated how the functional deterioration of T cells can affect host-microbiota symbiosis and gut barrier integrity and the implications of this deterioration for inflammaging, senescence, and health decline.

KLRG1 identifies regulatory T cells with mitochondrial alterations that accumulate with aging

Soto-Heredero G, Gabandé-Rodríguez E, Carrasco E, Escrig-Larena JI, Gómez de Las Heras MM, Delgado-Pulido S, Francos-Quijorna I, Blanco EM, Fernández-Almeida Á, Abia D, Rodríguez MJ, Fernández-Díaz CM, Álvarez-Flores MB, Ramírez de Molina A, Jung S, Del Sol A, Zorita V, Sánchez-Cabo F, Torroja C, Mittelbrunn M.

Nat Aging. 2025 Apr 30;

Online ahead of print.

  • PMID: 40307497
  • DOI: 10.1038/s43587-025-00855-9

Recent studies using single-cell RNA sequencing technology have uncovered several subpopulations of CD4+ T cells that accumulate with aging. These age-associated T cells are emerging as relevant players in the onset of inflammaging and tissue senescence. Here, based on information provided by single-cell RNA sequencing data, we present a flow cytometry panel that allows the identification

Butyrate extends health and lifespan in mice with mitochondrial deficiency

Gabandé-Rodríguez E, Gómez de Las Heras MM, Ramírez-Ruiz de Erenchun P, Simó C, García-Cañas V, Inohara N, Berenguer-López I, Enríquez-Zarralanga V, Fernández-Almeida Á, Oller J, Soto-Heredero G, Carrasco E, Delgado-Pulido S, Escrig-Larena JI, Francos-Quijorna I, Justo-Méndez R, Aranda JF, Poulton J, Lechuga-Vieco AV, Enríquez JA, Núñez G, Mittelbrunn M.

Nat Commun (2026).

  • PMID: 41826362
  • DOI: 10.1038/s41467-026-70547-4

Mitochondrial diseases progressively lead to multisystemic failure with treatment options remaining extremely limited. Here, to investigate strategies that alleviate mitochondrial dysfunction, we first generate a ubiquitous and tamoxifen-inducible knockout mouse model of mitochondrial transcription factor A (TFAM), a nuclear-encoded protein involved in mitochondrial DNA (mtDNA) maintenance — Tfamfl/flUbcCre-ERT2 (iTfamKO) mice. Systemic TFAM deficiency triggers mitochondrial decline in