2026-06-14T03:29:00Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/65142024-11-28T16:04:54Zcom_20.500.12105_19604com_20.500.12105_2051com_20.500.12105_15322col_20.500.12105_19605col_20.500.12105_16938col_20.500.12105_16980
Repisalud
author
Toribio-Fernandez, Raquel
author
Zorita, Virginia
author
Rocha-Perugini, Vera
author
Iborra, Salvador
author
Martinez del Hoyo, Gloria
author
Chevre, Raphael
author
Dorado, Beatriz
author
Sancho, David
author
Sanchez-Madrid, Francisco
author
Andres, Vicente
author
Gonzalez-Granado, Jose Maria
funder
Instituto de Salud Carlos III
funder
Fundación Ramón Areces
funder
Fondation ACTERIA (Acting on European Research in Immunology and Allergology)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Ministerio de Economía, Industria y Competitividad (España)
funder
Fundación ProCNIC
funder
Research Institute Hospital 12 de Octubre
2018-10-25T08:19:44Z
2018-10-25T08:19:44Z
2018
Cell Death Dis. 2018; 9(1):9
10.1038/s41419-017-0007-6
2041-4889
Cell Death and Disease
29311549
http://hdl.handle.net/20.500.12105/6514
Differentiation of naive CD4(+) T-cells into functionally distinct T helper (Th) subsets is critical to immunity against pathogen infection. Little is known about the role of signals emanating from the nuclear envelope for T-cell differentiation. The nuclear envelope protein lamin A/C is induced in naive CD4(+) T-cells upon antigen recognition and acts as a link between the nucleus and the plasma membrane during T-cell activation. Here we demonstrate that the absence of lamin A/C in naive T-cell reduces Th1 differentiation without affecting Th2 differentiation in vitro and in vivo. Moreover, Rag1(-/-) mice reconstituted with Lmna(-/-)CD4(+)CD25(-) T-cells and infected with vaccinia virus show weaker Th1 responses and viral removal than mice reconstituted with wild-type T-cells. Th1 responses and pathogen clearance upon Leishmania major infection were similarly diminished in mice lacking lamin A/C in the complete immune system or selectively in T-cells. Lamin A/C mediates Th1 polarization by a mechanism involving T-bet and IFN gamma production. Our results reveal a novel role for lamin A/C as key regulator of Th1 differentiation in response to viral and intracellular parasite infections.
eng
CD8(+) T-CELLS
CUTANEOUS LEISHMANIASIS
DENDRITIC CELLS
TRANSCRIPTION FACTOR
LINEAGE COMMITMENT
NUCLEAR-ENVELOPE
C57BL/6 MICE
C-FOS
IMMUNITY
EFFECTOR
Lamin A/C augments Th1 differentiation and response against vaccinia virus and Leishmania major
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