Requirement for CD40 Ligand in Costimulation Induction, T Cell Activation, and Experimental Allergic Encephalomyelitis

Science ◽  
1996 ◽  
Vol 273 (5283) ◽  
pp. 1864-1867 ◽  
Author(s):  
I. S. Grewal ◽  
H. G. Foellmer ◽  
K. D. Grewal ◽  
J. Xu ◽  
F. Hardardottir ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Experimental Allergic Encephalomyelitis ◽  
Cell Activation ◽  
Cd40 Ligand ◽  
Allergic Encephalomyelitis ◽  
Experimental Allergic

scholarly journals The immune response against myelin basic protein in two strains of rat with different genetic capacity to develop experimental allergic encephalomyelitis.

1975 ◽  
Vol 141 (1) ◽  
pp. 72-81 ◽  
Author(s):  
D E McFarlin ◽  
S C Hsu ◽  
S B Slemenda ◽  
F C Chou ◽  
R F Kibler
Keyword(s):  
Immune Response ◽  
T Cell ◽  
Experimental Allergic Encephalomyelitis ◽  
Cell Response ◽  
Basic Protein ◽  
T Cell Response ◽  
Skin Tests ◽  
Allergic Encephalomyelitis ◽  
Experimental Allergic

After challenge with guiena pig basic protein (GPBP) Lewis (Le) rats, which are homozygous for the immune response experimental allergic encephalomyelitis (Ir-EAE) gene, developed positive delayed skin tests against GPBP and the 43 residue encephalitogenic fragment (EF); in addition, Le rat lymph node cells (LNC) were stimulated and produced migration inhibitory factor (MIF) when incubated in vitro with these antigens. In contrast Brown Norway (BN) rats, which lack the Ir-EAE gene, did not develop delayed skin tests to EF and their LNC were not stimulated and did not produce MIF when incubated in vitro with EF. These observations indicate that the Ir-EAE gene controls a T-cell response against the EF. Le rats produced measurable anti-BP antibody by radioimmunoassay after primary challenge. Although no antibody was detectable in BN rats by radioimmunoassay, radioimmunoelectrophoresis indicated that a small amount of antibody was formed after primary immunization. After boosting intraperitoneally, both strains of rat exhibited a rise in anti-BP antibody; which was greater in Le rats. In both strains of rat the anti-BP antibody reacted with a portion of the molecule other than the EF. Since EF primarily evokes a T cell response, it is suggested that the EF portion of the BP molecule may contain a helper determinant in antibody production.

T cell receptors in autoimmune disease as targets for immune intervention

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 656-661 ◽  
Author(s):  
Hans Acha-Orbea ◽  
L. Steinman ◽  
H. O. McDevitt
Keyword(s):  
T Cell ◽  
Autoimmune Disease ◽  
T Cell Receptor ◽  
Experimental Allergic Encephalomyelitis ◽  
Antibody Therapy ◽  
Cell Receptor ◽  
Allergic Encephalomyelitis ◽  
Immune Intervention ◽  
Receptor Antibodies ◽  
Experimental Allergic

The optimal form of treatment for an autoimmune disease should be highly specific, have few side effects, and allow treatment of clinically apparent disease. One target that could fulfill these requirements is the T cell receptor. To answer the question whether treatment of autoimmune disesase is possible with anti-T cell receptor antibodies, the heterogeneity of T cell receptor elements utilized in the T cell mediated autoimmune disease experimental allergic encephalomyelitis was analyzed. The limited heterogeneity of these elements allowed prevention and treatment of clinical autoimmune disease with anti-T cell receptor monoclonal antibodies. These results and their potential value for other autoimmune diseases are discussed.Key words: T cell receptor, autoimmune disease, monoclonal antibody therapy, experimental allergic encephalomyelitis.

HgCl2-induced perturbation of the T cell network in experimental allergic encephalomyelitis

1991 ◽  
Vol 137 (2) ◽  
pp. 367-378 ◽  
Author(s):  
Jérôme Rossert ◽  
Lucette Pelletier ◽  
Régine Pasquier ◽  
Henri Villarroya ◽  
Rafael Oriol ◽  
...  
Keyword(s):  
T Cell ◽  
Experimental Allergic Encephalomyelitis ◽  
Allergic Encephalomyelitis ◽  
Cell Network ◽  
Experimental Allergic

scholarly journals A Critical Role for Cd40–Cd40 Ligand Interactions in Amplification of the Mucosal Cd8 T Cell Response

1999 ◽  
Vol 190 (9) ◽  
pp. 1275-1284 ◽  
Author(s):  
Leo Lefrançois ◽  
Sara Olson ◽  
David Masopust
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cd8 T Cells ◽  
Adoptive Transfer ◽  
Cell Activation ◽  
Cd8 T Cell ◽  
Cd40 Ligand ◽  
Interleukin 12 ◽  
Cd8 Cells

The role of CD40 ligand (CD40L) in CD8 T cell activation was assessed by tracking antigen-specific T cells in vivo using both adoptive transfer of T cell receptor transgenic T cells and major histocompatibility complex (MHC) class I tetramers. Soluble antigen immunization induced entry of CD8 cells into the intestinal mucosa and cytotoxic T lymphocyte (CTL) differentiation, whereas CD8 cells in secondary lymphoid tissue proliferated but were not cytolytic. Immunization concurrent with CD40L blockade or in the absence of CD40 demonstrated that accumulation of CD8 T cells in the mucosa was CD40L dependent. Furthermore, activation was mediated through CD40L expressed by the CD8 cells, since inhibition by anti-CD40L monoclonal antibodies occurred after adoptive transfer to CD40L-deficient mice. However, mucosal CD8 T cells in normal and CD40−/− mice were equivalent killers, indicating that CD40L was not required for CTL differentiation. Appearance of virus-specific mucosal, but not splenic, CD8 cells also relied heavily on CD40–CD40L interactions. The mucosal CTL response of transferred CD8 T cells was MHC class II and interleukin 12 independent. The results established a novel pathway of direct CD40L-mediated CD8 T cell activation.

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