TGFβ1 transduction enhances immunomodulatory capacity of neural stem cells in experimental autoimmune encephalomyelitis

Xie, Chong; Li, Xing; Zhou, Xiajun; Li, Zezhi; Zhang, Yuan; Zhao, Li; Hao, Yong; Zhang, Guang‐Xian; Guan, Yangtai

doi:10.1016/j.bbi.2017.11.023

Cited by 8 publications

(6 citation statements)

References 47 publications

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“…The EAE model was constructed as previously reported 19 : MOG 35‐55 (GL Biochem Ltd., Shanghai, China) was dissolved in PBS and then mixed with complete Freund's adjuvant (8 mg/mL) (strain H37RA; Difco, USA) at a 1:1 volume ratio. Female mice were injected with the emulsified solution at four sites.…”

Section: Methodsmentioning

confidence: 99%

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CD22 blockade aggravates EAE and its role in microglia polarization

Xiang,

Wang,

Han

et al. 2024

CNS Neurosci Ther

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AimsMultiple sclerosis (MS) is a neuroinflammatory demyelinating disease. Microglia are reportedly involved in the pathogenesis of MS. However, the key molecules that control the inflammatory activity of microglia in MS have not been identified.MethodsExperimental autoimmune encephalomyelitis (EAE) mice were randomized into CD22 blockade and control groups. The expression levels of microglial CD22 were measured by flow cytometry, qRT–PCR, and immunofluorescence. The effects of CD22 blockade were examined via in vitro and in vivo studies.ResultsWe detected increased expression of microglial CD22 in EAE mice. In addition, an in vitro study revealed that lipopolysaccharide upregulated the expression of CD22 in microglia and that CD22 blockade modulated microglial polarization. Moreover, an in vivo study demonstrated that CD22 blockade aggravated EAE in mice and promoted microglial M1 polarization.ConclusionCollectively, our study indicates that CD22 may be protective against EAE and may play a critical role in the maintenance of immune homeostasis in EAE mice.

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Section: Methodsmentioning

confidence: 99%

“…After fixation with 4% paraformaldehyde, the tissue was cut into 5‐μm‐thick sections. As reported previously, 19 hematoxylin and eosin (H&E) staining was carried out to assess the infiltration of inflammatory cells, while Luxol fast blue staining (LFB) staining was carried out to assess the severity of demyelination.…”

Section: Methodsmentioning

confidence: 99%

CD22 blockade aggravates EAE and its role in microglia polarization

Xiang,

Wang,

Han

et al. 2024

CNS Neurosci Ther

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“…Bone marrow-derived NSCs and those derived from the SVZ have been shown to exert almost the same therapeutic effects in the EAE preclinical models, and interestingly, the BM-derived NSCs have similar morphological characteristics and similar capability of differentiating into neurons and glial cells to SVZ-derived NSCs [ 344 ]. Xie et al injected bone marrow-derived NSC transfected with TGF-β1 into mice with EAE via the tail vein and transduced bone marrow-derived NSC inhibited Th1 and Th17 populations, promoting the production of immunosuppression through Treg cells and cytokine IL-10 from the periphery, thereby transforming microglia from a classical to an alternative pathway [ 345 ].…”

Section: Potential Ms Treatmentsmentioning

confidence: 99%

“…These results indicate that genetically modifying NSCs can be more effective at inhibiting clinical severity, inflammation, and demyelination in the CNS of mice. In addition, these investigations reported that the total number of neurons and oligodendrocytes in the CNS was significantly increased in the TGF-β1-transfected NSC transplantation group compared with the control group injected with normal saline [ 345 ]. However, there was no significant difference between the two groups treated with non-transfected NSCs when compared with the transfected NSC transplantation group.…”

Section: Potential Ms Treatmentsmentioning

confidence: 99%

The Heterogeneous Multiple Sclerosis Lesion: How Can We Assess and Modify a Degenerating Lesion?

Ellen

Nheu

et al. 2023

IJMS

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Multiple sclerosis (MS) is a heterogeneous disease of the central nervous system that is governed by neural tissue loss and dystrophy during its progressive phase, with complex reactive pathological cellular changes. The immune-mediated mechanisms that promulgate the demyelinating lesions during relapses of acute episodes are not characteristic of chronic lesions during progressive MS. This has limited our capacity to target the disease effectively as it evolves within the central nervous system white and gray matter, thereby leaving neurologists without effective options to manage individuals as they transition to a secondary progressive phase. The current review highlights the molecular and cellular sequelae that have been identified as cooperating with and/or contributing to neurodegeneration that characterizes individuals with progressive forms of MS. We emphasize the need for appropriate monitoring via known and novel molecular and imaging biomarkers that can accurately detect and predict progression for the purposes of newly designed clinical trials that can demonstrate the efficacy of neuroprotection and potentially neurorepair. To achieve neurorepair, we focus on the modifications required in the reactive cellular and extracellular milieu in order to enable endogenous cell growth as well as transplanted cells that can integrate and/or renew the degenerative MS plaque.

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“…For instance, NSCs may play a critical role in restoring balance between the adaptive lymphocytes Th17 and Tregs; Th17 restoration is accomplished through the inhibition of IL-6 expression (a pro-inflammatory cytokine inducing pathogenic Th17 cells for demyelination) and Th17/Treg balance is achieved through inhibition of TNF-α and IFN-γ 46 . NSCs’ therapeutic potential can be further enhanced by modulating factors like NT-3 (promoting remyelination through enhanced differentiation into oligodendrocytes and neurons while inhibiting differentiation into astrocytes), chemokine receptor-5 (promoting early-stage migration of NSCs to inflammatory foci) TGFβ-1 (upregulating Tregs and the microglial M2 phenotype while downregulating Th17 activity) and TGF-β2 (reprogramming infiltrative monocytes to anti-inflammatory myeloid cells) 32 , 34 , 37 , 38 . NSCs and MSCs show impressive potential for MS treatments and may also be beneficial in preventing later IS incidence by reducing neuroinflammation early.…”

Section: Stem Cell Therapies For Multiple Sclerosismentioning

confidence: 99%

Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review

et al. 2023

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The immense neuroinflammation induced by multiple sclerosis (MS) promotes a favorable environment for ischemic stroke (IS) development, making IS a deadly complication of MS. The overlapping inflammation in MS and IS is a prelude to the vascular pathology, and an inherent cell death mechanism that exacerbates neurovascular unit (NVU) impairment in the disease progression. Despite this consequence, no therapies focus on reducing IS incidence in patients with MS. To this end, the preclinical and clinical evidence we review here argues for cell-based regenerative medicine that will augment the NVU dysfunction and inflammation to ameliorate IS risk.

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TGFβ1 transduction enhances immunomodulatory capacity of neural stem cells in experimental autoimmune encephalomyelitis

Cited by 8 publications

References 47 publications

CD22 blockade aggravates EAE and its role in microglia polarization

CD22 blockade aggravates EAE and its role in microglia polarization

The Heterogeneous Multiple Sclerosis Lesion: How Can We Assess and Modify a Degenerating Lesion?

Stem Cells Attenuate the Inflammation Crosstalk Between Ischemic Stroke and Multiple Sclerosis: A Review

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