Frontiers in Cellular Neuroscience (Jul 2021)
Decreased Neurofilament L Chain Levels in Cerebrospinal Fluid and Tolerogenic Plasmacytoid Dendritic Cells in Natalizumab-Treated Multiple Sclerosis Patients – Brief Research Report
- Adriel S. Moraes,
- Vinicius O. Boldrini,
- Alliny C. Dionete,
- Marilia D. Andrade,
- Ana Leda F. Longhini,
- Ana Leda F. Longhini,
- Irene Santos,
- Amanda D. R. Lima,
- Veronica A. P. G. Silva,
- Rafael P. C. Dias Carneiro,
- Rafael P. C. Dias Carneiro,
- Rafael P. C. Dias Carneiro,
- Raphael P. S. Quintiliano,
- Breno B. Ferrari,
- Alfredo Damasceno,
- Fernando Pradella,
- Alessandro S. Farias,
- Alessandro S. Farias,
- Charles P. Tilbery,
- Renan B. Domingues,
- Renan B. Domingues,
- Carlos Senne,
- Carlos Senne,
- Gustavo B. P. Fernandes,
- Gustavo B. P. Fernandes,
- Felipe von Glehn,
- Carlos Otavio Brandão,
- Carlos Otavio Brandão,
- Carla R. A. V. Stella,
- Leonilda M. B. Santos,
- Leonilda M. B. Santos
Affiliations
- Adriel S. Moraes
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Vinicius O. Boldrini
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Alliny C. Dionete
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Marilia D. Andrade
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Ana Leda F. Longhini
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Ana Leda F. Longhini
- Department of Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, AL, United States
- Irene Santos
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Amanda D. R. Lima
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Veronica A. P. G. Silva
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Rafael P. C. Dias Carneiro
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Rafael P. C. Dias Carneiro
- Department of Neurology, University of Campinas, Campinas, Brazil
- Rafael P. C. Dias Carneiro
- MS Clinic of Santa Casa de São Paulo (CATEM), São Paulo, Brazil
- Raphael P. S. Quintiliano
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Breno B. Ferrari
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Alfredo Damasceno
- Department of Neurology, University of Campinas, Campinas, Brazil
- Fernando Pradella
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Alessandro S. Farias
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Alessandro S. Farias
- National Institute of Science and Technology on Neuroimmunomodulation (INCT-NIM), Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil
- Charles P. Tilbery
- MS Clinic of Santa Casa de São Paulo (CATEM), São Paulo, Brazil
- Renan B. Domingues
- MS Clinic of Santa Casa de São Paulo (CATEM), São Paulo, Brazil
- Renan B. Domingues
- Senne Liquor Diagnóstico, São Paulo, Brazil
- Carlos Senne
- Senne Liquor Diagnóstico, São Paulo, Brazil
- Carlos Senne
- Hospital Israelita Albert Einstein, São Paulo, Brazil
- Gustavo B. P. Fernandes
- Senne Liquor Diagnóstico, São Paulo, Brazil
- Gustavo B. P. Fernandes
- Hospital Israelita Albert Einstein, São Paulo, Brazil
- Felipe von Glehn
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Carlos Otavio Brandão
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Carlos Otavio Brandão
- Department of Neurology, University of Campinas, Campinas, Brazil
- Carla R. A. V. Stella
- Department of Neurology, University of Campinas, Campinas, Brazil
- Leonilda M. B. Santos
- Neuroimmunology Unit, Department of Genetics, Evolution, Microbiology, and Immunology, University of Campinas (UNICAMP), Campinas, Brazil
- Leonilda M. B. Santos
- National Institute of Science and Technology on Neuroimmunomodulation (INCT-NIM), Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil
- DOI
- https://doi.org/10.3389/fncel.2021.705618
- Journal volume & issue
-
Vol. 15
Abstract
BackgroundNeurofilament Light (NfL) chain levels in both cerebrospinal fluid (CSF) and serum have been correlated with the reduction of axonal damage in multiple sclerosis (MS) patients treated with Natalizumab (NTZ). However, little is known about the function of plasmacytoid cells in NTZ-treated MS patients.ObjectiveTo evaluate CSF NfL, serum levels of soluble-HLA-G (sHLA-G), and eventual tolerogenic behavior of plasmacytoid dendritic cells (pDCs) in MS patients during NTZ treatment.MethodsCSF NfL and serum sHLA-G levels were measured using an ELISA assay, while pDCs (BDCA-2+) were accessed through flow cytometry analyses.ResultsCSF levels of NfL were significantly reduced during NTZ treatment, while the serum levels of sHLA-G were increased. Moreover, NTZ treatment enhanced tolerogenic (HLA-G+, CD274+, and HLA-DR+) molecules and migratory (CCR7+) functions of pDCs in the peripheral blood.ConclusionThese findings suggest that NTZ stimulates the production of molecules with immunoregulatory function such as HLA-G and CD274 programmed death-ligand 1 (PD-L1) which may contribute to the reduction of axonal damage represented by the decrease of NfL levels in patients with MS.
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