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Novel Role for Macrophage Galactose-Type Lectin-1 to Regulate Innate Immunity against Mycobacterium tuberculosis
| Content Provider | Scilit |
|---|---|
| Author | Naqvi, Kubra F. Huante, Matthew B. Saito, Tais B. Endsley, Mark A. Gelman, Benjamin B. Endsley, Janice J. |
| Copyright Year | 2021 |
| Description | Tuberculosis (TB) caused by infection with Mycobacterium tuberculosis is characterized by inflammatory pathology and poorly understood mechanisms of innate immunity. Pattern recognition receptors, expressed on the surface of macrophages, determine the balance of inflammatory and antimicrobial functions that influence disease outcome. Carbohydrate moieties displayed by mycobacteria can serve as pattern recognition receptor ligands for some members of the C-type lectin receptor (CLR) family, interactions that mediate a variety of incompletely understood immune outcomes. This work identifies a novel role for the CLR macrophage galactose-type lectin (MGL)-1 in a mouse model (C57BL/6 and $MGL-1^{−/−}$) of experimental TB. Murine macrophages upregulated MGL-1 following in vitro exposure to M. tuberculosis, whereas $MGL^{+}$ cells accumulated at sites of mycobacteria-driven inflammation in the lung. Pulmonary macrophages from MGL-1–deficient mice displayed increased production of proinflammatory cytokines (IL-1β, IL-6, and IFN-γ) that were associated with greater lipid accumulation, following M. tuberculosis infection. Surprisingly, for a CLR, we also observed MGL-1–dependent antimycobacterial activity as evidenced by greater M. tuberculosis proliferation in bone marrow–derived macrophages, and the lung, of MGL-1–deficient mice. Differential transcriptome analysis further revealed that loss of MGL-1 perturbs the activation of various genes involved in the regulation of inflammation and lipid metabolism in the setting of M. tuberculosis infection. These results identify MGL-1 signaling as an important mechanism that regulates innate immunity against M. tuberculosis and indicates the potential for the MGL pathway as a novel therapeutic target for anti-TB immunity. |
| Ending Page | 233 |
| Page Count | 13 |
| Starting Page | 221 |
| ISSN | 00221767 |
| e-ISSN | 15506606 |
| DOI | 10.4049/jimmunol.2001276 |
| Journal | The Journal of Immunology |
| Issue Number | 1 |
| Volume Number | 207 |
| Language | English |
| Publisher | The American Association of Immunologists |
| Publisher Date | 2021-07-01 |
| Access Restriction | Open |
| Subject Keyword | C Type Lectin Receptor Macrophage Galactose-type Lectin (mgl) Innate Immunity |
| Content Type | Text |
| Resource Type | Article |
| Subject | Immunology and Allergy Immunology |
