Changes of B cell subsets in central pathological process of autoimmune encephalomyelitis in mice.

Changes of B cell subsets in central pathological process of autoimmune encephalomyelitis in mice.

Publication date: Jul 08, 2019

Multiple sclerosis is a demyelinating and autoimmune disease and its immune response is not fully elucidated. This study was conducted to examine the pathological changes and B cell subsets in experimental autoimmune encephalomyelitis (EAE) mice, and analyze the expression of triosephosphate isomerase (TPI) and GADPH to define the role of B cell subsets in the disease.

Female C57BL/6 mice were randomly divided into EAE group (n = 18) and control (n = 18). During the experiments, the weight and nerve function scores were determined. The proportions of B cell subsets in the peripheral blood were measured by flow cytometry. Seven, 18 and 30 days after immunization, the brain and spinal cord tissues were examined for the infiltration of inflammatory cells using hematoxylin-eosin (HE) HE staining and the demyelination using Luxol fast blue staining. The expression of B cell-related proteins was detected immunohistochemistrially and the expression of antigenic TPI and GADPH was analyzed using enzyme-linked immunosorbent assay (ELISA). HE staining showed that mice had more severe EAE 18 d than 7 d after modelling, while the symptoms were significantly relieved at 30 d. The results were consistent with the weight measurements and neural function scores. Immunohistochemistry studies showed that B cells aggregated in the spinal cord, but not much in the brain. Flow cytometry studies showed that there were more B cells in control than in EAE models from day 7 and the difference was narrowed at day 30. The level of plasma cells increased continuously, reached the top at day 21 and obviously declined at day 30. On other hand, the numbers of memory B cells increased gradually over the experimental period. The numbers of plasma and memory B cells were similar between the control and EAE mice. ELISA data revealed that the brain contents of TPI and GAPDH were higher in EAE mice than in control at day 7, while at day 18, the levels were reversed.

In the central pathological process of EAE mice, B cells exert role through the mechanism other than producing antibodies and the levels of brain TPI and GADPH are related to the severity of autoimmune induced-damage.

Open Access PDF

Xiong, Y., Cheng, S., Wu, X., Ren, Y., and Xie, X. Changes of B cell subsets in central pathological process of autoimmune encephalomyelitis in mice. 18541. 2019 BMC Immunol (20):1.

Concepts Keywords
Antibodies Immunization
Autoimmune Neurological disorders
Blood Organ systems
BMC Animal testing
Brain Experimental autoimmune encephalomyelitis
Demyelination Nervous system
ELISA EAE
Encephalomyelitis Multiple sclerosis
Eosin Transcription factors
Flow Cytometry Antibodies
GAPDH
Hematoxylin
Immunization
Immunohistochemistry
Memory
Mice
Multiple Sclerosis
Nerve
Plasma
Spinal Cord
Staining
TPI

Semantics

Type Source Name
gene UNIPROT ATP8A2
drug DRUGBANK ATP
gene UNIPROT BRD2
gene UNIPROT POMC
gene UNIPROT MSX2
gene UNIPROT FOXG1
gene UNIPROT TNIP1
gene UNIPROT KCTD11
gene UNIPROT REN
gene UNIPROT COL9A3
gene UNIPROT COMP
gene UNIPROT COL9A1
gene UNIPROT COL9A2
gene UNIPROT SCN8A
gene UNIPROT MBNL1
drug DRUGBANK Ocrelizumab
disease MESH syndromes
gene UNIPROT GTF2IRD1
gene UNIPROT CD3E
gene UNIPROT SALL1
gene UNIPROT TTC7A
drug DRUGBANK Tromethamine
gene UNIPROT ATM
gene UNIPROT SCN9A
drug DRUGBANK Water
gene UNIPROT FLNB
gene UNIPROT USO1
gene UNIPROT SEC14L2
gene UNIPROT NXF1
gene UNIPROT TNF
disease MESH dif
drug DRUGBANK Ethanol
gene UNIPROT RAN
drug DRUGBANK Ranitidine
gene UNIPROT CD27
gene UNIPROT IL2RA
gene UNIPROT ISG20
gene UNIPROT TUBE1
gene UNIPROT AK3
gene UNIPROT F9
drug DRUGBANK Formaldehyde
disease MESH death
disease MESH paralysis
gene UNIPROT JTB
gene UNIPROT NR1I2
gene UNIPROT TSPO
gene UNIPROT CHRM3
gene UNIPROT DUOXA1
gene UNIPROT KIT
gene UNIPROT PROC
gene UNIPROT APC
gene UNIPROT SDC1
gene UNIPROT CD19
gene UNIPROT PTPRC
gene UNIPROT CD4
gene UNIPROT C2
gene UNIPROT TALDO1
gene UNIPROT LRSAM1
pathway BSID Metabolism
gene UNIPROT FBLIM1
pathway BSID Pertussis
disease DOID pertussis
disease MESH pertussis
drug DRUGBANK Coenzyme M
gene UNIPROT LARGE1
gene UNIPROT CPSF4
gene UNIPROT DEPP1
gene UNIPROT GOPC
gene UNIPROT MOG
gene UNIPROT HLA-C
disease MESH inflammation
gene UNIPROT LAMC2
gene UNIPROT CSF2
drug DRUGBANK Rituximab
gene UNIPROT MBP
gene UNIPROT PRG2
gene UNIPROT MBL2
disease DOID myelitis
disease MESH myelitis
disease MESH sclerosis
gene UNIPROT MAGEE1
gene UNIPROT GAPDH
gene UNIPROT THOP1
gene UNIPROT FASTK
disease MESH demyelination
gene UNIPROT TPI1
drug DRUGBANK Tipiracil
disease MESH experimental autoimmune encephalomyelitis
disease DOID autoimmune disease
disease MESH autoimmune disease
disease DOID Multiple sclerosis
disease MESH Multiple sclerosis
disease DOID encephalomyelitis
disease MESH encephalomyelitis

Original Article

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