Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0014070 (
encephalomyelitis
)
13,017
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The CD28 co-stimulatory pathway is well established for T cell activation; however, results from CD28 -/- mice suggest the existence of additional co-stimulatory pathways. Here we report the further characterization of a new member of the CD2 superfamily,
NTB-A
, important in T cell co-stimulation.
NTB-A
is expressed on T cells, and its expression is up-regulated on activated cells. Triggering of
NTB-A
with monoclonal antibodies in the absence of CD28 signals leads to T cell proliferation and interferon-gamma secretion but not interleukin-4. Cross-linking of
NTB-A
also induces phosphorylation of
NTB-A
and the association of SAP (SLAM-associated protein), the protein absent in X-linked lymphoproliferative disease. T helper cells differentiated by cross-linking
NTB-A
and CD3 developed predominantly into Th1 cells not Th2 cells. In vivo blocking of
NTB-A
interactions with its ligands by using soluble
NTB-A
-Fc fusion protein inhibits B cell isotype switching to IgG2a and IgG3, commonly induced by Th1-type cytokines. Most important, treatment of mice with
NTB-A
-Fc delays the onset of antigen-induced experimental allergic
encephalomyelitis
in myelin basic protein-T cell receptor transgenic mice, suggesting a role in T cell-mediated autoimmune disease. Regulation of interferon-gamma secretion, and not interleukin-4 in vitro, as well as inhibition of Th1 cell-induced isotype switching and attenuation of experimental allergic
encephalomyelitis
indicate that
NTB-A
is important for Th1 responses. The observation that cross-linking of
NTB-A
induces T cell activation, expansion, and Th1-type cytokine production suggests
NTB-A
is a novel co-stimulatory receptor. The identification of
NTB-A
as a regulator of T cell response paves the way to provide novel therapeutic approaches for modulation of the immune response.
...
PMID:NTB-A, a new activating receptor in T cells that regulates autoimmune disease. 1498 14
