Identification of cellular factors associated with inflammation and neurodegeneration in multiple sclerosis

Serum biomarkers as neurofilament light chain (sNfL) and glial fibrillary acidic protein (sGFAP) enabled early identification of multiple sclerosis (MS) patients at risk of relapse-associated worsening (RAW) or progression independent of relapses (PIRA). However, the immunological mechanisms underly...

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Detalles Bibliográficos
Autores: Rodero-Romero, Alexander, Fernández Velasco, José Ignacio|||0000-0001-9148-671X, Monreal, Enric|||0000-0003-3293-0125, Sainz-Amo, Raquel, Alvarez-Lafuente, Roberto|||0000-0002-3132-1486, Comabella López, Manuel|||0000-0002-2373-6657, Ramió-Torrentà, Lluís|||0000-0002-6999-1004, García-Domínguez, José M., Villarrubia, Noelia, Sainz De La Maza, Susana, Domínguez-Mozo, María, Quiroga-Varela, Ana, Chico-García, Juan Luís, Rodriguez-Jorge, Fernando, Veiga-Gonzalez, José Luis, Roldán, Ernesto, Espiño, Mercedes, Rodríguez-Martín, Eulalia, Álvarez Bravo, Gary|||0000-0003-0342-0177, Masjuan, Jaime|||0000-0003-1329-0943, Montalban, Xavier|||0000-0002-0098-9918, Costa-Frossard, Lucienne|||0000-0002-6512-4413, Villar, Luisa M.|||0000-0002-9067-3668
Tipo de recurso: artículo
Fecha de publicación:2025
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:dnet:uabarcelona_::d2b6c6f5253717da91f591d366cf23d0
Acceso en línea:https://ddd.uab.cat/record/328387
https://dx.doi.org/urn:doi:10.3389/fimmu.2025.1648725
Access Level:acceso abierto
Palabra clave:Multiple sclerosis
Serum biomarkers
Cellular phenotype and function
Neurofilament light chain
Glial fibrillary acidic protein
Demyelinating disease of central nervous system
Descripción
Sumario:Serum biomarkers as neurofilament light chain (sNfL) and glial fibrillary acidic protein (sGFAP) enabled early identification of multiple sclerosis (MS) patients at risk of relapse-associated worsening (RAW) or progression independent of relapses (PIRA). However, the immunological mechanisms underlying these clinical phenotypes remain unclear. We conducted a cross-sectional study including 117 MS patients and 84 healthy controls (HC). Patients were stratified as NLGL (low sNfL and sGFAP), NH (high sNfL at different levels of sGFAP), and NLGH (low sNfL and high sGFAP). Percentages of blood and cerebrospinal fluid (CSF) mononuclear cells, and intracellular production of cytokines by T and B cells after " in vitro " stimulation were analyzed by flow cytometry. We identified a common inflammatory profile present in the blood of all MS groups comprising significant increases of effector CD4 + and CD8 + T cells, of memory and antigen-presenting B cells, of CD4 + and CD8 + T cells producing interferon-gamma, interleukin-17 and tumor necrosis factor-alpha (TNF-α) and of B cells producing TNF-α. Additionally, the highly inflammatory NH group showed lower frequencies of different regulatory subsets (transitional B cells, PDL1 + monocytes and Treg cells) compared to HC and increased percentages of CD4 + and CD8 + T cells producing granulocyte-macrophage colony-stimulating factor and of effector CD56 dim NK cells. They also showed lower percentages of Treg in blood and CSF compared to the low inflammatory NLGL group, which also displayed higher frequencies of regulatory CD56 dim, NKG2A + cells. All MS patients share increased inflammatory B and T cells, but differ in regulatory or NK subsets, which identify highly inflammatory or benign disease courses.

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