<p>In this study, we tested whether type I interferons (IFN-I), namely IFN-alpha and IFN-beta, may promote <i>Mycobacterium tuberculosis</i> (Mtb) pathogenesis by exacerbating cell death of human monocyte-derived macrophages (MDM) infected with Mtb. We differentiated the MDM under two different published methods (see Document Method.pdf for Table 1 of Methods). To determine if MDM infected with Mtb upregulates IFN-I transcripts, signaling factors, or IFN-I stimulated genes (ISGs), the MDM were infected with Mtb or treated with an activator of stimulator of IFN genes (STING), diamidobenzimidazole (di-ABZI). STING activation acted as a positive control for IFN-I induction and ISG upregulation. Indeed, di-ABZI treated MDM differentiated under both methods upregulated ISGs 24 hpi. At 24 hour post treatment, MDM differentiated under one method, but not under another method, upregulated ISGs, such as <a href="https://www.ncbi.nlm.nih.gov/gene/9636">ISG15</a>, <a href="https://www.ncbi.nlm.nih.gov/gene/10410">IFITM3</a>, and <a href="https://www.ncbi.nlm.nih.gov/gene/3627">CXCL10</a>, upon Mtb infection. MDM differentiated under both methods upregulated ISGs upon di-ABZI treatment.</p>

Type I Interferon Exacerbates Mycobacterium Tuberculosis Induced Human    Macrophage Death

Mycobacterium tuberculosis study with RNA-Seq data on dbGaP (3 participants)

Type I Interferon Exacerbates Mycobacterium Tuberculosis Induced Human Macrophage Death

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