| First Author | Barman PK | Year | 2019 |
| Journal | J Immunol | Volume | 202 |
| Issue | 9 | Pages | 2720-2727 |
| PubMed ID | 30910860 | Mgi Jnum | J:274634 |
| Mgi Id | MGI:6296962 | Doi | 10.4049/jimmunol.1801481 |
| Citation | Barman PK, et al. (2019) Skin Wounding-Induced Monocyte Expansion in Mice Is Not Abrogated by IL-1 Receptor 1 Deficiency. J Immunol 202(9):2720-2727 |
| abstractText | The aim of this study was to determine whether skin wounding induces monocyte (Mo) expansion in bone marrow and whether IL-1R1 signaling regulates this process. Our data show that skin wounding increases myeloid lineage-committed multipotent progenitors (MPP3 subset) and Mo in bone marrow, but this expansion is not impaired in Il1r1(-/-) mice. We also demonstrate that M-CSF-induced differentiation of myeloid progenitors into Mo is not impaired by the loss of IL-1R1 ex vivo, indicating that IL-R1 deficiency does not abrogate myeloid progenitor differentiation potential. In addition, we observed modestly delayed wound closure in Il1r1(-/-) mice associated with higher frequency of Ly6C(lo) Mo in the circulation at baseline and in wounds early after injury. Thus, in contrast to other models of inflammation that involve IL-1R1-dependent monopoiesis, our results demonstrate that skin wounding induces Mo progenitor and Mo expansion independently of IL-1R1 signaling. |
