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This Service

A database built with INDRA combining content from numerous readers and databases. This page allows you to curate the loaded statements. For more information please see the manual.

This Project

INDRA is developed by indralabs, a part of the Harvard Medical School Laboratory of Systems Pharmacology.

This project, indra_db, is also developed by the indralab team. For more information on how we procure our sources, you can go here. This work was funded by ARO grant W911NF‐15‐1‐0544 under the DARPA Communicating with Computers program.

IndraLab

Statements

TNFAIP3 decreases the amount of IL17A. 2 / 2

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"Together, these data suggest that TNFα signaling via TNFR2 promotes the expression of the anti-inflammatory mediator TNFAIP3/A20, which seems to prevent IL-17A expression in regulatory T cells, as ablation of TNFα signaling suppresses TNFAIP3/A20 and results in increased IL-17A expression in human Treg."

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"Functional blockage of TNFAIP3 in normal CD4 + T cells using small interfering RNA increased the expression of IFN-gamma and IL-17, but not IL-2, IL-4 and IL-5."

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Our Sources:

INDRA allows us to combine the results from a multitude of sources. In particular, the INDRA Database draws on the following...