Resident murine alveolar and peritoneal macrophages differ in adhesion of apoptotic thymocytes

Apoptotic cells must be cleared efficiently by macrophages (Mcircle divide) to prevent autoimmunity, yet their ingestion impairs Mcircle divide microbicidal function. The principal murine resident lung phagocyte, the alveolar Mcircle divide (AMcircle divide), is specifically deficient at apoptotic cell ingestion, both in vitro and in vivo, compared with resident peritoneal Mcircle divide (PMcircle divide). To further characterize this deficiency, we assayed static adhesion in vitro using apoptotic thymocytes and resident AMcircle divide and PMcircle divide from normal C57BL/6 mice. Adhesion of apoptotic thymocytes by both types of Mcircle divide was rapid, specific, and cold-sensitive. Antibody against the receptor tyrosine kinase MerTK (Tyro12) blocked phagocytosis but not adhesion in both types of Mcircle divide. Surfactant protein A increased adhesion and phagocytosis by AMcircle divide, but not to the levels seen using PMcircle divide. Adhesion was largely cation-independent for PMcircle divide and calcium-dependent for AMcircle divide. Adhesion was not inhibited in either Mcircle divide type by mAbs against beta1 or beta3 integrins or scavenger receptor I/II (CD204), but AMcircle divide adhesion was inhibited by specific mAbs against CD11c/CD18. Thus, resident m urine tissue Mcircle divide from different tissues depend on qualitatively disparate receptor systems to bind apoptotic cells. The decreased capacity of murine AMcircle divide to ingest apoptotic cells is only partially explained by reduced initial adhesion.