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1.
Neurosci Bull ; 35(3): 507-518, 2019 Jun.
Article in English | MEDLINE | ID: mdl-30796753

ABSTRACT

Myasthenia gravis (MG) is a prototypical antibody-mediated neurological autoimmune disease with the involvement of humoral immune responses in its pathogenesis. T follicular helper (Tfh) cells have been implicated in many autoimmune diseases. However, whether and how Tfh cells are involved in MG remain unclear. Here, we established and studied a widely-used and approved animal model of human MG, the rat model with acetylcholine receptor alpha (AChRα) subunit (R-AChR97-116)-induced experimental autoimmune myasthenia gravis (EAMG). This model presented mild body-weight loss 10 days after the first immunization (representing the early stage of disease) and more obvious clinical manifestations and body-weight loss 7 days after the second immunization (representing the late stage of disease). AChR-specific pre-Tfh cells and mature Tfh cells were detected in these two stages, respectively. In co-cultures of Tfh cells and B cells, the number of IgG2b-secreting B cells and the level of anti-AChR antibodies in the supernatant were higher in the cultures containing EAMG-derived Tfh cells. In immunohistochemistry and immunofluorescence assays, a substantial number of CD4+/Bcl-6+ T cells and a greater number of larger germinal centers were observed in lymph node tissues resected from EAMG rats. Based on these results, we hypothesize that an AChR-specific Tfh cell-mediated humoral immune response contributes to the development of EAMG.


Subject(s)
Immunity, Humoral , Myasthenia Gravis, Autoimmune, Experimental/immunology , Receptors, Cholinergic/immunology , T-Lymphocytes, Helper-Inducer/immunology , Animals , B-Lymphocytes/immunology , Disease Models, Animal , Female , Lymph Nodes/immunology , Protein Subunits/immunology , Proto-Oncogene Proteins c-bcl-6/immunology , Rats, Inbred Lew , Receptor Cross-Talk
2.
Clin Immunol ; 173: 109-116, 2016 Dec.
Article in English | MEDLINE | ID: mdl-27664932

ABSTRACT

MicroRNA 182 has been found to have a distinct contribution in the clonal expansion of activated- and functioning of specialized-helper T cells. In this study we knocked down microRNA 182 in vivo and induced experimental autoimmune encephalomyelitis (EAE) to determine the influences of microRNA 182 in the Treg cells functional specialization through Foxo1 dependent pathway in the peripheral lymphoid organs. Down-regulation of microRNA 182 significantly increased the proportions of Foxp3+ T cells in the peripheral lymph nodes and spleen. In vivo study verified a positive correlation between microRNA 182 levels and symptom severity of EAE, and a negative correlation between microRNA 182 and the transcriptional factor Foxp3. In vitro polarization study also confirmed the contribution of Foxo1 in microRNA 182 mediated down-regulation of Foxp3+ T cells. Together, our results provide evidence that during the development of EAE, microRNA 182 repressed Treg cells differentiation through the Foxo1 dependent pathway.


Subject(s)
Encephalomyelitis, Autoimmune, Experimental/immunology , Forkhead Box Protein O1/immunology , MicroRNAs/immunology , T-Lymphocytes, Regulatory/immunology , Animals , Cell Differentiation , Female , Lymph Nodes/cytology , Mice, Inbred C57BL , Spleen/cytology , T-Lymphocytes, Regulatory/physiology
3.
Immunology ; 138(4): 333-45, 2013 Apr.
Article in English | MEDLINE | ID: mdl-23181351

ABSTRACT

Experimental allergic encephalomyelitis (EAE) can be induced in animal models by injecting the MOG35-55 peptide subcutaneously. Dendritic cells (DCs) that are located at the immunization site phagocytose the MOG35-55 peptide. These DCs mature and migrate into the nearest draining lymph nodes (dLNs), then present antigen, resulting in the activation of naive T cells. T helper type 1 (Th1) and Th17 cells are the primary cells involved in EAE progression. All-trans-retinoic acid (AT-RA) has been shown to have beneficial effects on EAE progression; however, whether AT-RA influences DC maturation or mediates other functions is unclear. In the present study, we showed that AT-RA led to the down-regulation of MHC class II, CD80 (B7-1) and CD86 (B7-2) expressed on the surface of DCs that were isolated from dLNs or spleen 3 days post-immunization in an EAE model. Changes to DC function influenced Th1/Th17 subset polarization. Furthermore, the number of CD44(+) monocytes (which might trigger EAE progression) was also significantly decreased in dLNs, spleen, subarachnoid space and the spinal cord parenchyma after AT-RA treatment. These findings are the first to demonstrate that AT-RA impairs the antigen-presenting capacity of DCs, leading to down-regulation of pathogenic Th1 and Th17 inflammatory cell responses and reducing EAE severity.


Subject(s)
Antioxidants/therapeutic use , Dendritic Cells/drug effects , Encephalomyelitis, Autoimmune, Experimental/drug therapy , Monocytes/drug effects , Tretinoin/therapeutic use , Animals , Antigen Presentation/drug effects , Antigens, CD/genetics , Antigens, CD/immunology , Antioxidants/pharmacology , Cell Differentiation/drug effects , Dendritic Cells/immunology , Dendritic Cells/pathology , Encephalomyelitis, Autoimmune, Experimental/chemically induced , Encephalomyelitis, Autoimmune, Experimental/immunology , Encephalomyelitis, Autoimmune, Experimental/pathology , Female , Gene Expression Regulation/drug effects , Histocompatibility Antigens Class II/genetics , Histocompatibility Antigens Class II/immunology , Immunization , Lymph Nodes/drug effects , Lymph Nodes/immunology , Lymph Nodes/pathology , Mice , Mice, Inbred C57BL , Monocytes/immunology , Monocytes/pathology , Myelin-Oligodendrocyte Glycoprotein , Peptide Fragments , Signal Transduction/drug effects , Spinal Cord/drug effects , Spinal Cord/immunology , Spinal Cord/pathology , Spleen/drug effects , Spleen/immunology , Spleen/pathology , Th1 Cells/drug effects , Th1 Cells/immunology , Th1 Cells/pathology , Th17 Cells/drug effects , Th17 Cells/immunology , Th17 Cells/pathology , Tretinoin/pharmacology
4.
Cancer Biol Ther ; 12(7): 610-6, 2011 Oct 01.
Article in English | MEDLINE | ID: mdl-21785272

ABSTRACT

The relationship between IL-17A and cancer, whether beneficial or antagonistic, continues to be a controversial issue. In this study, effects of IL-17A on lung adenocarcinoma were investigated using lung cancer cell lines, 95D and 95C. In the presence or absence of IL-17A, cell proliferation and VEGF secretion were detected. Effects of IL-17A on capillary networks and process of angiogenesis were also evaluated. In vivo, the level of IL-17A was assayed in the serum of lung adenocarcinoma patients. At the same time, slices of adenocarcinoma tissue were analyzed for expression of IL-17A, its receptor (IL-17RA), VEGF, CD4(+)-IL-17A+ cells and CD8(+)-IL-17A+ cells by immunohistochemistry and immunofluorescence assays. IL-17A did not have effect on the proliferation of 95D or 95C cells, however, the elevated expression of VEGF in supernatant of 95D or 95C cells was found to be IL-17A concentration-dependent. Supernatants from 95D or 95C cells treated with IL-17A could obviously facilitate angiogenesis, compared with IL-17A absence group (P < 0.01). Higher levels of IL-17A were detected in serum of patients with lung adenocarcinoma than healthy controls (P < 0.001). Higher positive expressions of IL-17A, IL-17RA and VEGF were confirmed in lung adenocarcinoma lesion tissues compared to pericancerous normal tissues (P < 0.001). Tnc17 cells, as well as Th17 cells were found in adenocarcinoma tissue, indicating a potential role of these cells in disease. In summary, IL-17A might affect lung adenocarcinoma by promoting angiogenesis, while the role of Tnc17 cells or Th17 cells remains to be elucidated.


Subject(s)
Adenocarcinoma/metabolism , Interleukin-17/metabolism , Lung Neoplasms/metabolism , Adenocarcinoma/drug therapy , Adenocarcinoma/pathology , Adenocarcinoma of Lung , Adult , Aged , CD4 Antigens/metabolism , CD8 Antigens/metabolism , Cell Line, Tumor , Cell Proliferation , Endothelial Cells/drug effects , Endothelial Cells/pathology , Female , Humans , Interleukin-17/blood , Interleukin-17/pharmacology , Lung Neoplasms/drug therapy , Lung Neoplasms/pathology , Male , Middle Aged , Neovascularization, Pathologic/chemically induced , Receptors, Interleukin-17/metabolism , Reference Values , Vascular Endothelial Growth Factor A/metabolism
5.
Neurosci Lett ; 497(2): 128-33, 2011 Jun 22.
Article in English | MEDLINE | ID: mdl-21539896

ABSTRACT

The aim of this present study is to evaluate the therapeutic effect of co-transplantation of neuregulin-1-transfected Schwann cells (SCs) and bone marrow stromal cells (BMSCs) on a rat model of spinal cord hemi-section injuries (Brown-Séquard syndrome), which is relevant to human clinical spinal cord injury. Both in vivo and in vitro data we received demonstrated that co-transplantation BMSCs with NRG1-transfected SCs reduced the size of cystic cavities, promoted axonal regeneration and hind limb functional recovery in comparison with SCs or BMSCs transplantation alone or together, and this treatment could provide important insights into potential therapies of spinal cord hemi-section injuries.


Subject(s)
Bone Marrow Cells/physiology , Bone Marrow Transplantation/methods , Neuregulin-1/genetics , Schwann Cells/transplantation , Spinal Cord Injuries/therapy , Animals , Cysts/pathology , Cysts/therapy , Disease Models, Animal , Female , Male , Neuregulin-1/physiology , Rats , Rats, Wistar , Schwann Cells/physiology , Spinal Cord Injuries/pathology , Stromal Cells/physiology , Stromal Cells/transplantation , Syndrome , Transfection/methods
6.
J Neuroimmunol ; 220(1-2): 25-33, 2010 Mar 30.
Article in English | MEDLINE | ID: mdl-20117842

ABSTRACT

Successive electroacupuncture (EA) stimulation on Zusanli ST36 acupoints of rats with experimental autoimmune encephalitis (EAE), which is an inflammatory disease mediated by autoreactive T cells, relieved disease severity, inhibited specific T cell proliferation and rebuilt the CD4+ T cell subset balance. In addition, EA-treated rats had significantly higher ACTH concentrations in vivo compared to untreated EAE rats. These results indicated that EA stimulation could relieve the severity of EAE by restoring balance to the Th1/Th2/Th17/Treg Th cell subset responses by stimulating the hypothalamus to increase ACTH secretion.


Subject(s)
Electroacupuncture/methods , Encephalomyelitis, Autoimmune, Experimental/immunology , Encephalomyelitis, Autoimmune, Experimental/therapy , Immune Tolerance/physiology , Immunosuppression Therapy/methods , T-Lymphocytes/immunology , Acupuncture Points , Adrenocorticotropic Hormone/blood , Adrenocorticotropic Hormone/metabolism , Animals , Cell Count , Cell Proliferation , Chemotaxis, Leukocyte/immunology , Disease Models, Animal , Encephalomyelitis, Autoimmune, Experimental/physiopathology , Female , Hypothalamus/metabolism , Lymphocyte Activation/immunology , Rats , Rats, Inbred Lew , T-Lymphocytes, Helper-Inducer/immunology , T-Lymphocytes, Helper-Inducer/metabolism , T-Lymphocytes, Regulatory/immunology , T-Lymphocytes, Regulatory/metabolism , Th1 Cells/immunology , Th1 Cells/metabolism , Th2 Cells/immunology , Th2 Cells/metabolism , Treatment Outcome
7.
J Neuroimmunol ; 212(1-2): 17-25, 2009 Jul 25.
Article in English | MEDLINE | ID: mdl-19457561

ABSTRACT

Interleukin-17 (IL-17) is active in a variety of brain injuries, including ischemia. The objective of this study was to test the hypothesis that IL-17 potentiates neuronal injury after stroke. Increased expression of IL-17 and IL-17 receptor (IL-17R) in serum and cortex was evaluated by ELISA, RT-PCR and immunohistochemistry. In the in vitro model of oxygen-glucose deprivation (OGD), IL-17 showed a dose-dependent effect in promoting neuronal injury through IL-17-IL-17R combination which can be blocked by IL-17R/Fc chimera. Our results demonstrated the up-regulation of IL-17 and IL-17R following permanent middle cerebral artery occlusion and suggested that they contributed to stroke outcome.


Subject(s)
Brain Ischemia/pathology , Cell Hypoxia , Glucose/metabolism , Interleukin-17/physiology , Neurons/pathology , Receptors, Interleukin-17/physiology , Animals , Apoptosis , Cells, Cultured , Hippocampus/pathology , Humans , Interleukin-17/analysis , Interleukin-17/genetics , Male , Mice , Mice, Inbred C57BL , Receptors, Interleukin-17/analysis , Receptors, Interleukin-17/genetics
8.
Brain Res ; 1271: 74-82, 2009 May 19.
Article in English | MEDLINE | ID: mdl-19332040

ABSTRACT

The parafascicular thalamic nucleus (nPf) is a critical relay in the ascending system that mediates motor control in the central nervous system (CNS). Yet, little is known about whether or not the nPf is involved in the development of morphine dependence and withdrawal. In the present study, kainic acid was used to chemically destroy the nPf in Wistar rats, and morphine dependence and withdrawal models were established. Morphine withdrawal symptoms score was evaluated in each group. An electrophysiological method was used to measure the changes in spontaneous discharge of nPf neurons. mu-Opioid receptor (MOR) mRNA level in nPf was detected using semi-quantitative RT-PCR. The ultrastructural alterations were examined by transmission electron microscopy. Results showed that the bilateral lesion of nPf had a marked influence on the development of morphine dependence and withdrawal. In order to address the mechanisms underlying, we found: (1) the average frequency and sum of nPf neurons that exhibited spontaneous discharge were increased in the morphine withdrawal group in comparison with the sham model group (P<0.05); (2) MOR mRNA level in the nPf of the morphine dependence group was decreased in comparison with that of the sham model group (1.45+/-0.38 vs. 5.37+/-0.94, P<0.01). In the morphine withdrawal group, which underwent 40 h withdrawal, the MOR mRNA level was higher than that in the morphine dependence group (2.97+/-0.73 vs. 1.45+/-0.38, P<0.05) but still lower than that in the sham model group (P<0.05); (3) the ultrastructural injuries of nPf neurons, which were in the nucleus, organelles and neuropil, were marked in the morphine dependent and withdrawal groups. Our study indicated that nPf played an important role in the development of morphine dependence and withdrawal. The results suggest that nPf may become a therapeutic target for treating morphine withdrawal syndrome.


Subject(s)
Intralaminar Thalamic Nuclei/drug effects , Intralaminar Thalamic Nuclei/pathology , Morphine Dependence/pathology , Morphine/pharmacology , Substance Withdrawal Syndrome/pathology , Animals , Cell Nucleus/drug effects , Cell Nucleus/metabolism , Cell Nucleus/pathology , Denervation , Disease Models, Animal , Electrophysiology , Intralaminar Thalamic Nuclei/physiopathology , Kainic Acid , Male , Microscopy, Electron, Transmission , Morphine Dependence/metabolism , Morphine Dependence/physiopathology , Narcotics/pharmacology , Nerve Degeneration/chemically induced , Nerve Degeneration/pathology , Nerve Degeneration/physiopathology , Neurons/drug effects , Neurons/pathology , Neurotoxins , Organelles/drug effects , Organelles/metabolism , Organelles/pathology , RNA, Messenger/drug effects , RNA, Messenger/metabolism , Rats , Rats, Wistar , Receptors, Opioid, mu/genetics , Reverse Transcriptase Polymerase Chain Reaction , Substance Withdrawal Syndrome/metabolism , Substance Withdrawal Syndrome/physiopathology
9.
Eur J Immunol ; 39(3): 800-9, 2009 Mar.
Article in English | MEDLINE | ID: mdl-19283707

ABSTRACT

In addition to their capacity to differentiate, BM stromal cells (BMSC) have immunosuppressive qualities that make them strong candidates for use in cell therapy against human autoimmune diseases. We studied the immunoregulatory activities of BMSC on experimental autoimmune myasthenia gravis (EAMG) in vitro and in vivo. Intravenous administration of syngenic BMSC to EAMG-model rats on the day of their second immunization was effective in ameliorating the pathological features of the disease. In vitro, the proliferative ability of T cells or B cells from EAMG rats was inhibited when they were cocultured with BMSC at proper ratios. This inhibitory effect was at least partially dependent on the secretion of IDO. We also determined that the development of EAMG is accompanied by an imbalance among the Th1, Th2, Th17, and Treg cell subsets, and that this can be corrected by the administration of BMSC, which leads to an increase of Th2 (IL-4) and Treg (Foxp3) cells, and a reduction of Th1 (IFN-gamma) and Th17 (IL-17) cells, through an IDO-dependent mechanism. These results provide further insights into the pathogenesis of MG, EAMG, and other immune-mediated diseases, and support a potential role for BMSC in their treatment.


Subject(s)
Bone Marrow Cells/immunology , Cytokines/immunology , Indoleamine-Pyrrole 2,3,-Dioxygenase/immunology , Myasthenia Gravis, Autoimmune, Experimental/immunology , Stromal Cells/immunology , Animals , B-Lymphocytes/immunology , B-Lymphocytes/metabolism , Bone Marrow Cells/metabolism , Cytokines/biosynthesis , Female , Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism , Myasthenia Gravis, Autoimmune, Experimental/chemically induced , Myasthenia Gravis, Autoimmune, Experimental/metabolism , Peptides/pharmacology , Rats , Rats, Inbred Lew , Stromal Cells/metabolism , T-Lymphocytes, Helper-Inducer/immunology , T-Lymphocytes, Helper-Inducer/metabolism , T-Lymphocytes, Regulatory/immunology , T-Lymphocytes, Regulatory/metabolism
10.
J Neuroimmunol ; 207(1-2): 83-91, 2009 Feb 15.
Article in English | MEDLINE | ID: mdl-19174310

ABSTRACT

Bone marrow stromal cells (BMSCs) are strong candidates for cell therapy against human autoimmune diseases. Intravenous administration of syngenic BMSCs to EAMG-model rats effectively ameliorated the disease, partially through a TGF-beta-dependent mechanism. The proliferative ability of T or B cells from EAMG rats was inhibited by BMSCs at proper cocultured ratios. And the imbalance of Th1, Th2, Th17 and Treg cell subsets accompanied with the development of EAMG was corrected by the administration of BMSCs. These results provide further insights into the pathogenesis of MG, EAMG, and other immune-mediated diseases, and support a potential role for BMSCs in their treatment.


Subject(s)
Bone Marrow Transplantation/methods , Myasthenia Gravis, Autoimmune, Experimental/surgery , Stromal Cells/transplantation , T-Lymphocytes, Helper-Inducer/metabolism , T-Lymphocytes, Regulatory/metabolism , Transforming Growth Factor beta/metabolism , Animals , B-Lymphocytes/immunology , B-Lymphocytes/metabolism , Body Weight , Cell Proliferation , Coculture Techniques/methods , Cytokines/metabolism , Disease Models, Animal , Female , Immunoglobulins/metabolism , Myasthenia Gravis, Autoimmune, Experimental/immunology , Peptides/immunology , Rats , Rats, Inbred Lew , Receptors, Cholinergic/immunology , Stromal Cells/immunology , T-Lymphocytes, Helper-Inducer/classification , T-Lymphocytes, Helper-Inducer/immunology , T-Lymphocytes, Regulatory/immunology , Time Factors , Transforming Growth Factor beta/immunology
11.
Neurosci Lett ; 445(1): 117-21, 2008 Nov 07.
Article in English | MEDLINE | ID: mdl-18782604

ABSTRACT

To determine whether the receptor for advanced glycation endproducts (RAGE) contributes to cerebral ischemia, we evaluated RAGE expression in human cerebral ischemia and a model of permanent middle cerebral artery occlusion (pMCAO) in rats. Biopsy specimens were obtained from 12 patients with unilateral cerebral infarction. For the pMCAO model, the middle cerebral artery (MCA) of Sprague-Dawley (SD) rats was permanently occluded. Immunohistochemistry and Western blotting were used to measure RAGE expression in the ischemic hemisphere relative to the normal hemisphere. PC12 cells subjected to oxygen and glucose deprivation (OGD) were used to evaluate the role of RAGE in cell injury. As expected, cerebral ischemia patients expressed elevated levels of RAGE in the ischemic hemisphere. In 1 and 2 days pMCAO rats, levels of RAGE were higher in the ischemic hemisphere relative to the non-ischemic hemisphere, and expression was primarily located in the penumbra of the ischemic hemisphere. In PC12 cells, levels of RAGE increased after 7h of OGD culture. Notably, blockade of RAGE with a selective RAGE antibody in vitro reduced the cytotoxicity caused by OGD. The present data suggest that RAGE is up-regulated in human cerebral ischemia and pMCAO rats, suggesting a role for RAGE in brain ischemia.


Subject(s)
Brain Ischemia/pathology , Cerebral Cortex/metabolism , Infarction, Middle Cerebral Artery/pathology , Receptors, Immunologic/metabolism , Up-Regulation/physiology , Adult , Aged , Animals , Brain Ischemia/complications , Cell Count , Disease Models, Animal , Female , Humans , Male , Middle Aged , PC12 Cells , Rats , Rats, Sprague-Dawley , Receptor for Advanced Glycation End Products , Receptors, Immunologic/genetics , Time Factors
12.
Int J Pharm ; 352(1-2): 29-35, 2008 Mar 20.
Article in English | MEDLINE | ID: mdl-18053659

ABSTRACT

This study is concerned with preparing PLGA nanoparticles loaded with voriconazole (PNLV), investigating the burst release and agglomeration of PNLV, and also evaluating antifungal efficacy of PNLV compared with voriconazole (VRC). The emulsion-solvent evaporation technique for nanoparticles and tests against fungi were completed. The amount of VRC in PNLV with sodium hexametaphosphate was 2.01+/-0.27%, and burst release of PNLV was reduced by about 33% using 20% ethanol solution (n=3). The mean D(50) of PNLV with or without this salt was 132.8 nm and 6.3 microm, respectively (n=5). In vitro; the fungal numbers treated with PNLV (3.5 mg/ml, equal amount calculated by VRC) and VRC (70 microg/ml) in tubes at the day 7 were 5.74 log(10) and 6.72 log(10), respectively (P<0.05). In vivo; the fungal burden treated with PNLV and VRC in tissue from mice kidneys at day 7 after administration was 0.64 log(10) and 2.61 log(10), respectively (5 mg/kg, P<0.001). The hematoxylin-eosin stain in mice kidney showed that the pathological lesions treated with PNLV were relieved in contrast with those with VRC. These results suggest that the emulsion-solvent evaporation process is feasible in preparing PNLV. Moreover, ethanol solution decreased burst release and Na-HMP inhibited agglomeration. PNLV could improve the VRC antifungal efficacy.


Subject(s)
Antifungal Agents/chemistry , Drug Carriers , Nanoparticles , Polyglactin 910/chemistry , Pyrimidines/chemistry , Triazoles/chemistry , Animals , Antifungal Agents/pharmacology , Candida albicans/drug effects , Candida albicans/growth & development , Chemistry, Pharmaceutical , Drug Compounding , Ethanol/chemistry , Feasibility Studies , Kidney/drug effects , Kidney/microbiology , Kinetics , Mice , Particle Size , Phosphates/chemistry , Pyrimidines/pharmacology , Solubility , Solvents/chemistry , Surface Properties , Technology, Pharmaceutical/methods , Triazoles/pharmacology , Voriconazole
13.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi ; 23(8): 737-40, 2007 Aug.
Article in Chinese | MEDLINE | ID: mdl-17618568

ABSTRACT

AIM: To investigate the effect and immuoregulative mechanisms of NK1.1(+) cells on the development of experimental autoimmune myasthenia gravis (EAMG). METHODS: The NK1.1(+) cells were depleted by intraperitoneal (i.p.) administration of anti-mouse NK1.1 mAb to C57BL/6 mice. Mice were immunized subcutaneously with AChR in CFA. The incidence and severity of EAMG was determined according to the Lennon disease symptoms grading. IFN-gamma and IL-4 in MNCs culture medium were measured by ELISA. AChR IgG of serum was measured by radioimmunoassay. In some experiments, the anti-IFN-gamma mAb was injected (i.p.) to neutralize IFN-gamma. RESULTS: The onset of EAMG was delayed and the severity was decreased obviously in NK1.1(+) cell-depleted mice. However, depletion of NK1.1(+) cells after immunization had no impact on the development of EAMG. Depletion of NK1.1(+) cells could significantly reduce the expression of AChR-specific antibody as well as the production of IFN-gamma. The development of EAMG and production of AChR specific Ab in NK1.1(+) cell-depleted mice were decreased obviously after treating with anti-IFN-gamma antibody. CONCLUSION: NK1.1(+) cells are involved in the early EAMG, and NK1.1(+) cells could enhance the production of IFN-gamma released by AChR-specific T cells as well as the AChR-specific antibodies, which may enhance the outcome of EAMG.


Subject(s)
Killer Cells, Natural/immunology , Myasthenia Gravis, Autoimmune, Experimental/immunology , Animals , Antibodies/immunology , Antibodies/pharmacology , Enzyme-Linked Immunosorbent Assay , Female , Interferon-gamma/immunology , Interferon-gamma/metabolism , Interleukin-4/metabolism , Killer Cells, Natural/physiology , Mice , Mice, Inbred BALB C , Myasthenia Gravis, Autoimmune, Experimental/chemically induced , Myasthenia Gravis, Autoimmune, Experimental/pathology , Radioimmunoassay , Random Allocation , Receptors, Nicotinic/immunology
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