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A study from the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, USA has reported that “Host-directed therapy of tuberculosis based on interleukin-1 and type I interferon crosstalk.”

This study was published in the June 25, 2014 Nature by Prof. Sher, Mayer-Barber Katrin D and others from the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, USA.

On the foundation of this interesting finding, Dr L Boominathan, Director-cum-chief Scientist of GBMDreports here that: Insights into the treatment of Tuberculosis: Tumor suppressor p33(ING1b) inhibits the pathogenesis and progression of tuberculosis (Mtb) via up regulation of its target gene.  This study suggests that p33(ING1b), by down regulating its target gene, it may increase the levels of lipid inflammatory mediator Prostaglandin E2. Thereby, it  inhibits the pathogenesis and progression of tuberculosis. Together, this study suggests that pharmacological formulations encompassing “p33(ING1b) or its activators” can be used to inhibit the progression of tuberculosis. 

Idea Proposed/Formulated by: Dr L Boominathan PhD

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CitationBoominathan, Insights into the treatment of Tuberculosis: Tumor suppressor p33(ING1b) inhibits the pathogenesis and progression of tuberculosis (Mtb) via up regulation of its target gene, 17/July/2014, 6.08 am,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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