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Hisgatlas

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Hisgatlas

What's it?

HisgAtlas is a manual curation database for human immunosuppression genes. Immunosuppression is body’s state in which the activation or efficacy of immune system is weakened. It is associated with a wide spectrum of human diseases, such as autoimmune diseases, allergy, organ transplantation rejection and chronic infectious diseases. In the last two decades, tremendous efforts have been made to elucidate the mechanism of hundreds of immunosuppression genes. For example, The programmed cell death-1 (PD-1) receptor, a cell surface receptor on T cells，which plays a critical role in peripheral tolerance, can also compromise antiviral and antitumor T cell responses through the inhibition of T cell proliferation. Blockade of the PD-1/PD-L1 pathway can active antitumor immune responses and have been a very successful therapy for cancer. Immunosuppression genes could be valuable drug targets or biomarkers for the immunotherapeutic treatment of different diseases. However, the information of all previously identified immunosuppression genes is dispersed in thousands of publications. Here we provided the HisgAtlas database that collects 995 previously identified human immunosuppression genes using text mining and manual curation.

Link

http://biokb.ncpsb.org/hisgatlas/

How to use it?

Users may search HisgAtlas in two ways. Users can input a gene name in the "Gene Name" search box and a drop-down menu will provide auto-completed genes stored in the database. Selecting one of them and clicking the "Search" button will lead to the queried results containing a table showing the immunosuppression genes, their associated diseases as well as the supporting evidence. All current query terms will be deleted if users click the "Reset" button. Users can input a disease name in the "Disease Term" search box, and a drop-down menu will provide auto-completed diseases stored in the database. Selecting one of them and clicking the "Search" button will lead to the queried results containing a table showing the immunosuppression associated diseases, their effector genes as well as the supporting literature evidence.

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