RT journal article
T1 Expression of Non-T Cell Activation Linker (NTAL) in Jurkat Cells Negatively Regulates TCR Signaling: Potential Role in Rheumatoid Arthritis
A1 Narbona Sánchez,  Isaac
A1 Pérez Linaza, Alba
A1 Serrano García, Isabel
A1 Vico Barranco, Inmaculada
A1 Fernández Aguilar, Luis Miguel
A1 Poveda Díaz, José L.
A1 Sánchez del Pino, María Jesús
A1 Medina Varo, Fermín
A1 Martínez de Arbulo Echevarría, Miguel
A1 Aguado Vidal, Enrique
A2 BiomedicinaBiotecnología y Salud Pública
K1 rheumatoid arthritis
K1 LAB
K1 LAT2
K1 NTAL
K1 signaling
K1 TCR
AB T lymphocytes are key players in adaptive immune responses through the recognition of peptide antigens through the T Cell Receptor (TCR). After TCR engagement, a signaling cascade is activated, leading to T cell activation, proliferation, and differentiation into effector cells. Delicate control of activation signals coupled to the TCR is needed to avoid uncontrolled immune responses involving T cells. It has been previously shown that mice deficient in the expression of the adaptor NTAL (Non-T cell activation linker), a molecule structurally and evolutionarily related to the transmembrane adaptor LAT (Linker for the Activation of T cells), develop an autoimmune syndrome characterized by the presence of autoantibodies and enlarged spleens. In the present work we intended to deepen investigation into the negative regulatory functions of the NTAL adaptor in T cells and its potential relationship with autoimmune disorders. For this purpose, in this work we used Jurkat cells as a T cell model, and we lentivirally transfected them to express the NTAL adaptor in order to analyze the effect on intracellular signals associated with the TCR. In addition, we analyzed the expression of NTAL in primary CD4+ T cells from healthy donors and Rheumatoid Arthritis (RA) patients. Our results showed that NTAL expression in Jurkat cells decreased calcium fluxes and PLC-γ1 activation upon stimulation through the TCR complex. Moreover, we showed that NTAL was also expressed in activated human CD4+ T cells, and that the increase of its expression was reduced in CD4+ T cells from RA patients. Our results, together with previous reports, suggest a relevant role for the NTAL adaptor as a negative regulator of early intracellular TCR signaling, with a potential implication in RA.
PB MDPI
SN 1661-6596
YR 2023
FD 2023-02-26
LK http://hdl.handle.net/10498/31826
UL http://hdl.handle.net/10498/31826
LA eng
DS Repositorio Institucional de la Universidad de Cádiz
RD 08-nov-2026