| First Author | Mayer-Barber KD | Year | 2011 |
| Journal | Immunity | Volume | 35 |
| Issue | 6 | Pages | 1023-34 |
| PubMed ID | 22195750 | Mgi Jnum | J:179275 |
| Mgi Id | MGI:5301734 | Doi | 10.1016/j.immuni.2011.12.002 |
| Citation | Mayer-Barber KD, et al. (2011) Innate and Adaptive Interferons Suppress IL-1alpha and IL-1beta Production by Distinct Pulmonary Myeloid Subsets during Mycobacterium tuberculosis Infection. Immunity 35(6):1023-34 |
| abstractText | Interleukin-1 (IL-1) receptor signaling is necessary for control of Mycobacterium tuberculosis (Mtb) infection, yet the role of its two ligands, IL-1alpha and IL-1beta, and their regulation in vivo are poorly understood. Here, we showed that both IL-1alpha and IL-1beta are critically required for host resistance and identified two multifunctional inflammatory monocyte-macrophage and DC populations that coexpressed both IL-1 species at the single-cell level in lungs of Mtb-infected mice. Moreover, we demonstrated that interferons (IFNs) played important roles in regulating IL-1 production by these cells in vivo. Type I interferons inhibited IL-1 production by both subsets whereas CD4(+) T cell-derived IFN-gamma selectively suppressed monocyte-macrophages. These data provide a cellular basis for both the anti-inflammatory effects of IFNs and probacterial functions of type I IFNs during Mtb infection and reveal differential regulation of IL-1 production by distinct cell populations as an additional layer of complexity in the activity of IL-1 in vivo. |
