title: [B cell activation in experimental autoimmune myasthenia graves treated with Talpha146-162-iMDCs].
abstract: OBJECTIVE
  To explore the therapic effect of Talpha146-162- iMDCs in C57BL/6 mice with experimental autoimmune myasthenia graves (EAMG), and illustrate whether this therapic effect is related with the change of B cells activation.
  
  
  METHODS
  Adult male C57BL/6 mice were randomly divided into EAMG groups(A), the prevention group(B) and control group(C); Immature bone marrow dendritic cells were cultured and pulsed with Talpha146-162. Mice of A group and B group were evaluated for clinical score till the day they were put to death. The expression and phosphorylation of Syk, Lyn, Btk and PLC-gamma2 protein were measured by Western blot.
  
  
  RESULTS
  75% mice of A group and 25% mice of B group were developed the accumulated incidence, the difference was significant (P<0.05). The average clinical score of A group and B group were 1.69+/-1.12 vs 0.35+/-0.67(P<0.01) at the termination of experiment. The expression and phosphorylation of Syk and PLC-gamma2 protein in spleen and lymphonode of the mice of A group were higher than those of C group (P<0.01) and B group (P< 0.05). Compared with C group, those of B group were higher (P<0.05); The expression and phosphorylation of Lyn protein in spleen and lymphonode of the mice of A (P<0.01) and B (P<0.05) groups were lower than those of C group. Compared with A group, those of B group were higher (P<0.05); The expression of Btk protein in spleen and lymphonode of the mice of A (P<0.01) and B (P<0.05) groups were higher than those of C group. And those of B groups were lower than those of A group (P<0.05). But there were no remarkable differences among the phosphorylation of Btk protein of three groups.
  
  
  CONCLUSIONS
  Talpha146-162-iMDCs can prevent EAMG and probably ameliorate EAMG by the negative regulation on BCR signaling.
authors.affiliation: Department of Neurology, Xiangya Hospital, Central South University, Changsha, China. dlian72@sina.com
authors.forename: Rong
authors.initials: R
authors.lastname: Wang
authors.forename: Huan
authors.initials: H
authors.lastname: Yang
authors.forename: Bo
authors.initials: B
authors.lastname: Xiao
authors.forename: Li-Fang
authors.initials: LF
authors.lastname: Zhang
mesh_terms: D000077329:Agammaglobulinaemia Tyrosine Kinase; D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D003713:Dendritic Cells / Q000276:immunology; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D008198:Lymph Nodes / Q000378:metabolism; D008213:Lymphocyte Activation / Q000276:immunology*; D008211:Lymphocyte Cooperation / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D020720:Myasthenia Gravis, Autoimmune, Experimental / Q000276:immunology* / Q000628:therapy*; D051966:Phospholipase C gamma / Q000378:metabolism; D010766:Phosphorylation; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D011897:Random Allocation; D011978:Receptors, Nicotinic / Q000276:immunology*; D013154:Spleen / Q000378:metabolism; D000072377:Syk Kinase; D013601:T-Lymphocytes / Q000276:immunology*; D019061:src-Family Kinases / Q000378:metabolism
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D011978:Receptors, Nicotinic; D011505:Protein-Tyrosine Kinases; D000077329:Agammaglobulinaemia Tyrosine Kinase; D000072377:Syk Kinase; C000606897:Syk protein, mouse; C060902:lyn protein-tyrosine kinase; D019061:src-Family Kinases; D051966:Phospholipase C gamma