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Review
. 2022 Oct 26:16:1028653.
doi: 10.3389/fncel.2022.1028653. eCollection 2022.

Glial cells and neurologic autoimmune disorders

Zhao-Qing Li  1 , Tong-Xin Li  1 , Miao Tian  1 , Ze-Sheng Ren  1 , Chen-Yi Yuan  1 , Rui-Kun Yang  1 , Su-Juan Shi  1 , Hui Li  1 , Zhen-Zhen Kou  1
Affiliations
Review

Glial cells and neurologic autoimmune disorders

Zhao-Qing Li et al. Front Cell Neurosci. .

Abstract

Neurologic autoimmune disorders affect people's physical and mental health seriously. Glial cells, as an important part of the nervous system, play a vital role in the occurrence of neurologic autoimmune disorders. Glial cells can be hyperactivated in the presence of autoantibodies or pathological changes, to influence neurologic autoimmune disorders. This review is mainly focused on the roles of glial cells in neurologic autoimmune disorders and the influence of autoantibodies produced by autoimmune disorders on glial cells. We speculate that the possibility of glial cells might be a novel way for the investigation and therapy of neurologic autoimmune disorders.

Keywords: Guillain–Barre syndrome; autoantibody; glial cells; multiple sclerosis; myelin oligodendrocyte glycoprotein antibody-related diseases; neurologic autoimmune disorders; neuromyelitis optica spectrum disorders.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
The pathogenesis of MS. Multiple sclerosis (MS) is an autoimmune disease characterized by chronic inflammation, demyelination, and gliosis in the CNS. At the early stage of MS, microglia could be activated and proliferated, which act as antigen-presenting cells. M1 microglia are differentiated by IFN-γ and LPS, secreting IL-12 and IL-23, promoting the differentiation of Th1 cells and Th 17 cells, leading to the aggravation of the inflammatory response of MS. M2 microglia are activated by IL-4/IL-13 and play a role in anti-inflammation. Macrophages have similar functions as microglia, including the presentation of antigens and cytokines production. M1 macrophages have the antigen-presenting ability the same as M1 microglia, resulting in the demyelination of nerves in MS. M2 macrophages increases Th2 cell differentiation to protect oligodendrocytes and neurons from damage. In MS, astrocytes can be activated, enhancing the permeability of BBB, and recruiting lymphocytes into the CNS. Moreover, astrocytes participate in the formation of BBB and secret immune inhibitory factors, acting in an anti-inflammatory role. The resting astrocytes inhibit the proliferation and promote apoptosis of Th1 cells and promote the secretion of anti-inflammatory cytokines by Th2 cells. Oligodendrocytes form the myelin sheath of CNS axons, providing nutrition and protecting nerve axons. At the early stage of MS, the regeneration and self-healing of nerve myelin sheath lesions are completed by the differentiation of OPCs into mature oligodendrocytes, but the differentiation ability is finally lost in progressive MS.
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