Pathogenesis of acute passive murine encephalomyelitis: II. Th1 phenotype of the inducing population is not sufficient to cause disease

This publication has 31 references indexed in Scilit:

• Myelin Basic Protein–specific T Helper 2 (Th2) Cells Cause Experimental Autoimmune Encephalomyelitis in Immunodeficient Hosts Rather than Protect Them from the Disease
  The Journal of Experimental Medicine, 1997
• CD28/B7 Regulation of Th1 and Th2 Subsets in the Development of Autoimmune Diabetes
  Published by Elsevier ,1996
• Lymphoproliferative Disorders with Early Lethality in Mice Deficient in Ctla-4
  Science, 1995
• Loss of CTLA-4 leads to massive lymphoproliferation and fatal multiorgan tissue destruction, revealing a critical negative regulatory role of CTLA-4
  Immunity, 1995
• Cytokines and Murine Autoimmune Encephalomyelitis: Inhibition or Enhancement of Disease with Antibodies to Select Cytokines, or by Delivery of Exogenous Cytokines Using a Recombinant Vaccinia Virus System
  Scandinavian Journal of Immunology, 1995
• Encephalitogenic Th1 cells are inhibited by Th2 cells with related peptide specificity: Relative roles of interleukin (IL)-4 and IL-10
  Journal of Neuroimmunology, 1993
• Surface expression of alpha 4 integrin by CD4 T cells is required for their entry into brain parenchyma.
  The Journal of Experimental Medicine, 1993
• Encephalitogenic T cells in the B10.PL model of experimental allergic encephalomyelitis (EAE) are of the Th-1 lymphokine subtype
  Cellular Immunology, 1989
• TH1 and TH2 Cells: Different Patterns of Lymphokine Secretion Lead to Different Functional Properties
  Annual Review of Immunology, 1989
• The rapid isolation of clonable antigen‐specific T lymphocyte lines capable of mediating autoimmune encephalomyelitis
  European Journal of Immunology, 1981