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NFIL3 deficiency alleviates EAE through regulating different immune cell subsets.

Zhigang Chen1, Rong Fan2, Jie Liang3

  • 1Department of Neurology, The Third Affiliated Hospital, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong 510630, PR China; Department of Neurology, The Fifth Affiliated Hospital, Sun Yat-sen University, 52 Meihua East Road, Zhuhai, Guangdong 519000, PR China; Department of Clinical Immunology, The Third Affiliated Hospital, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong 510630, PR China.

Journal of Advanced Research
|July 1, 2022
PubMed
Summary
This summary is machine-generated.

NFIL3 deficiency alleviates experimental autoimmune encephalomyelitis (EAE) by altering immune cell populations. This impacts T cells and dendritic cells, reducing central nervous system inflammation and demyelination.

Keywords:
AutoimmunityDendritic cellsEAENFIL3T cells

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Area of Science:

  • Immunology
  • Neuroscience
  • Molecular Biology

Background:

  • Nuclear factor, iridin-like 3 (NFIL3) influences immune system components.
  • NFIL3 is implicated in the function and development of various immune cell subsets.
  • Experimental autoimmune encephalomyelitis (EAE) involves immune cells and causes central nervous system (CNS) inflammation and demyelination.

Purpose of the Study:

  • To investigate the role of NFIL3 in EAE pathogenesis.
  • To analyze the impact of NFIL3 on T cells and dendritic cells (DCs) during EAE.
  • To explore the crosstalk between T cells and DCs in the context of NFIL3 deficiency.

Main Methods:

  • Established MOG35-55-induced EAE in NFIL3 knockout and wildtype mice.
  • Monitored clinical scores and analyzed immune cell populations via flow cytometry.
  • Assessed neuroinflammation and demyelination using histology and evaluated DC-T cell interactions in vitro.

Main Results:

  • NFIL3 deficiency led to decreased Th17 cells in the CNS, reduced clinical scores, and milder neuroinflammation/demyelination.
  • In NFIL3 knockout mice, peripheral CD4+ T cells showed increased PD-1 and ICOS, with decreased Th2, Th9, CD8+CD103+, and GM-CSF+ CD4+ T cells.
  • NFIL3-deficient CD11c+ dendritic cells exhibited impaired pro-inflammatory and enhanced anti-inflammatory functions.

Conclusions:

  • NFIL3 deficiency ameliorates MOG35-55-induced EAE by modulating adaptive and innate immunity.
  • The protective effect involves regulating T cell subsets and dendritic cell function.
  • NFIL3 plays a critical role in the immune cell crosstalk, particularly between CD4+ T cells and CD11c+ dendritic cells, during EAE.