Acta Neuropathologica: The reason why MS has less protrusion glial cell differentiation block: exogente immunocytokines, not endogenesis less dexterity glial cytokines.

Multiple sclerosis (MS) is the most common central nervous system inflammation and demyelination disorder in Central and North America.
the symptoms depend on the site and severity of multiple sclerosis in the brain and spinal cord, which vary greatly, but usually includes numbness in the limbs, vision problems and fatigue.
most patients (approximately 80%) begin with a recurrence-remission (RR) course, characterized by an acute exacerbation period, followed by a full or partial recovery.
, despite significant advances in immunotherapy on MS, progress in the disease remains unsuppressed.
promotes re-myelinization is an endo-type repair mechanism that forms a new myelin around the demyelination axon and is a promising new treatment.
, however, in MS lesions, re-myelinization often fails, which may be due in part to the differentiation of less progenitic cells into mature, less protrusive glial cells with myelin.
is not clear why MS patients have less protrusion glial differentiation damage and re-myelinization defects.
In order to determine whether the internal less protrusion glial cytokines lead to the re-formation of damaged myelin in relapsed-remission-relieving multiple sclerosis (RRMS), we compared adhesive stem cell-sourced less dextinent glial cells (hiOL) from RRMS patients and control groups, where two single-egg twins were inconsistent with multiple sclerosis.
Method: The team of authors reviewed samples of paraffin encephalitis in 32 MS patients, histologically characterized by inflammatory demyelination, who underwent surgery after extensive clinical diagnosis to rule out tumors or infectious diseases.
study was approved by the University of Minnesota Ethics Committee, all methods were conducted in accordance with the relevant guidelines and regulations, and all patients received informed consent for surgery.
found that hiOL in RRMS patients and the control group were almost indesotic in terms of remedification-related functions and proteomic composition.
, however, when analyzing the effects of exogenous factors, we found that the serum of a single nuclear cell (PBMCs) of active exomenemia significantly inhibited the differentiation of less dexterous glial cells.
, we determined that CD4-T cells are media that are damaged by the differentiation of less protruding glial cells, at least in part because of interferon secretion.
In addition, we also observed that the application of differentiation-promoting drugs could not restore the small dexterous glial cell differentiation disorder induced by liquidation on PBMC, while the treatment of PBMCs with the immunomodulated drug Teflonide was partially saved before the collection of supernatant fluid.
summary, these data show that less protrusion glial differentiation block is not due to the inherent less protrusion glial factors, but is caused by the inflammatory environment in RRMS lesions, which requires consideration of the inflammatory environment of drug screening methods.
these findings may help develop new strategies to promote re-myelinization.
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