Searching across hundreds of databases

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

The surface protein TIGIT suppresses T cell activation by promoting the generation of mature immunoregulatory dendritic cells.

Nature immunology | Jan 17, 2009

Here we have identified a surface protein, TIGIT, containing an immunoglobulin variable domain, a transmembrane domain and an immunoreceptor tyrosine-based inhibitory motif that was expressed on regulatory, memory and activated T cells. Poliovirus receptor, which is expressed on dendritic cells, bound TIGIT with high affinity. A TIGIT-Fc fusion protein inhibited T cell activation in vitro, and this was dependent on the presence of dendritic cells. The binding of poliovirus receptor to TIGIT on human dendritic cells enhanced the production of interleukin 10 and diminished the production of interleukin 12p40. Knockdown of TIGIT with small interfering RNA in human memory T cells did not affect T cell responses. TIGIT-Fc inhibited delayed-type hypersensitivity reactions in wild-type but not interleukin 10-deficient mice. Our data suggest that TIGIT exerts immunosuppressive effects by binding to poliovirus receptor and modulating cytokine production by dendritic cells.

Pubmed ID: 19011627 RIS Download

Mesh terms: Amino Acid Sequence | Animals | CHO Cells | Cell Communication | Cell Differentiation | Cells, Cultured | Cricetinae | Cricetulus | Dendritic Cells | Down-Regulation | Humans | Immune Tolerance | Immunologic Memory | Interleukin-10 | Interleukin-12 Subunit p40 | Membrane Proteins | Mice | Mice, Inbred C57BL | Molecular Sequence Data | Protein Binding | Receptors, Immunologic | Receptors, Virus | Sequence Alignment | T-Lymphocytes

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

Associated grants

None

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.

We have not found any resources mentioned in this publication.