GPR30 FORMS AN INTEGRAL PART OF E2-PROTECTIVE PATHWAY IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS

Lignende værker

• Estrogen-induced protection against experimental encephalomyelitis is abrogated in the absence of B cells
  af: Bodhankar, Sheetal, et al.
  Udgivet: (2011)
• GPR30, but not estrogen receptor-α, is crucial in the treatment of experimental autoimmune encephalomyelitis by oral ethinyl estradiol
  af: Yates, Melissa A, et al.
  Udgivet: (2010)
• Oestrogen treatment of experimental autoimmune encephalomyelitis requires 17β-oestradiol-receptor-positive B cells that up-regulate PD-1 on CD4(+) Foxp3(+) regulatory T cells
  af: Bodhankar, Sheetal, et al.
  Udgivet: (2012)
• Oestrogen-mediated protection of experimental autoimmune encephalomyelitis in the absence of Foxp3(+) regulatory T cells implicates compensatory pathways including regulatory B cells
  af: Subramanian, Sandhya, et al.
  Udgivet: (2011)
• T Lymphocytes Do Not Directly Mediate the Protective Effect of Estrogen on Experimental Autoimmune Encephalomyelitis
  af: Polanczyk, Magdalena J., et al.
  Udgivet: (2004)