<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16</volume><submitter>Browning SE</submitter><pubmed_abstract>&lt;i>Mycobacterium tuberculosis&lt;/i> (Mtb) and HIV are leading infectious causes of death worldwide and act synergistically to worsen disease during co-infection. C-type lectin receptors (CLR) respond to pathogen-associated carbohydrates to activate downstream innate immunity and can be exploited for entry of intracellular pathogens. The macrophage (MΦ) galactose-type lectin (MGL, CLEC10A) is an immunomodulatory CLR associated with M2 MΦ. We previously described an immune role for a murine MGL homologue in an experimental model of tuberculosis (TB). Herein we extend these findings by identifying human MGL as an important member of the Mtb-responsive pathogen recognition receptor (PRR) repertoire that is activated in both M1 and M2 polarizing conditions. MΦ exposure to Mtb activates MGL expres</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1597281</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12522201</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>MGL/CLEC10A is an important C-type lectin receptor activated in the innate immune response to &amp;lt;i&amp;gt;Mycobacterium tuberculosis&amp;lt;/i&amp;gt; and is suppressed in people with HIV.</pubmed_title><pmcid>PMC12522201</pmcid><pubmed_authors>Chauhan S</pubmed_authors><pubmed_authors>Huante MB</pubmed_authors><pubmed_authors>Martinez-Martinez YB</pubmed_authors><pubmed_authors>Fan X</pubmed_authors><pubmed_authors>Gelman BB</pubmed_authors><pubmed_authors>Paez RN</pubmed_authors><pubmed_authors>Endsley MA</pubmed_authors><pubmed_authors>Naqvi KF</pubmed_authors><pubmed_authors>Lisinicchia JG</pubmed_authors><pubmed_authors>Nguyen H</pubmed_authors><pubmed_authors>Holloway AJ</pubmed_authors><pubmed_authors>Browning SE</pubmed_authors><pubmed_authors>Bharaj P</pubmed_authors><pubmed_authors>Endsley JJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>MGL/CLEC10A is an important C-type lectin receptor activated in the innate immune response to &amp;lt;i&amp;gt;Mycobacterium tuberculosis&amp;lt;/i&amp;gt; and is suppressed in people with HIV.</name><description>&lt;i>Mycobacterium tuberculosis&lt;/i> (Mtb) and HIV are leading infectious causes of death worldwide and act synergistically to worsen disease during co-infection. C-type lectin receptors (CLR) respond to pathogen-associated carbohydrates to activate downstream innate immunity and can be exploited for entry of intracellular pathogens. The macrophage (MΦ) galactose-type lectin (MGL, CLEC10A) is an immunomodulatory CLR associated with M2 MΦ. We previously described an immune role for a murine MGL homologue in an experimental model of tuberculosis (TB). Herein we extend these findings by identifying human MGL as an important member of the Mtb-responsive pathogen recognition receptor (PRR) repertoire that is activated in both M1 and M2 polarizing conditions. MΦ exposure to Mtb activates MGL expres</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-06-04T12:04:38.108Z</modification><creation>2026-05-09T03:07:40.33Z</creation></dates><accession>S-EPMC12522201</accession><cross_references><pubmed>41103425</pubmed><doi>10.3389/fimmu.2025.1597281</doi></cross_references></HashMap>