| First Author | Rocha-Resende C | Year | 2021 |
| Journal | J Mol Cell Cardiol | Volume | 157 |
| Pages | 98-103 | PubMed ID | 33971183 |
| Mgi Jnum | J:311417 | Mgi Id | MGI:6715022 |
| Doi | 10.1016/j.yjmcc.2021.05.003 | Citation | Rocha-Resende C, et al. (2021) B cells modulate the expression of MHC-II on cardiac CCR2(-) macrophages. J Mol Cell Cardiol 157:98-103 |
| abstractText | The uninjured murine heart contains a heterogeneous population of macrophages with disparate ontogenies and functions. These macrophages are often associated with blood vessels and can be subclassified based on the expression of CC chemokine receptor 2 (CCR2) and major histocompatibility complex class II (MHC-II). The biological cues that modulate these macrophage pool subpopulations have not been completely identified. It has been recently shown that a sub-population of circulating naive B cells adheres to the myocardial microvasculature. We hypothesized that B cells might modulate the phenotype of myocardial macrophages. To test this hypothesis, we analyzed both the relative location of B cells and macrophages in myocardial histological section and the prevalence of myocardial macrophage subsets in hearts from B cell-deficient mice (muMT) and mice depleted of B cells through administration of an anti-CD20 antibody. We found that B cells pause in the microvasculature in proximity of macrophages and modulate the number of myocardial CCR2(-)MHC-II(high) cells. Through in vitro studies we found that this is likely the result of a paracrine effect of B cells on the expression of MHC-II in CCR2(-) cells. These results reveal an unexpected relationship between B cells and resident macrophages and, highlighting a direct intramyocardial effect of circulating B cells, challenge the currently held belief that naive recirculating B lymphocytes merely shuttle between lymphoid stations. |
