F4/80 as a Major Macrophage Marker: The Case of the Peritoneum and Spleen

Abstract

Tissue macrophages are a heterogeneous cell population residing in all body tissues that contribute to the maintenance of homeostasis and trigger immune activation in response to injurious stimuli. This heterogeneity may be associated with tissue-specific functions; however, the presence of distinct macrophage populations within the same microenvironment indicates that macrophage heterogeneity may also be influenced outside of tissue specialization. The F4/80 molecule was established as a unique marker of murine macrophages when a monoclonal antibody was found to recognize an antigen exclusively expressed by these cells. However, recent research has shown that F4/80 is expressed by other immune cells and is not equivalently expressed across tissue-specific macrophage lineages, including those residing in the same microenvironment, such as the peritoneum and spleen. In this context, two murine macrophage subtypes with distinct F4/80 expression patterns were recently found to coexist in the peritoneum, termed large peritoneal macrophages (LPMs) and small peritoneal macrophages (SPMs). However, the presence of phenotypic and functional heterogeneous macrophage subpopulations in the spleen was already known. Thus, although F4/80 surface expression continues to be the best method to identify tissue macrophages, additional molecules must also be examined to distinguish these cells from other immune cells.

Elevated Levels of Interleukin-27 in Early Life Compromise Protective Immunity in a Mouse Model of Gram-Negative Neonatal Sepsis

“…We recently described MDSCs as a significant source of IL-27 (12), and it is tempting to speculate that these cells are a significant source of rising levels during infection. F4/80 is expressed in monocytes, macrophages, and eosinophils (54,55). An unexpected finding was that the frequency of these cells was not increased in septic pups.…”

Particulate Matter Increases the Severity of Bleomycin-Induced Pulmonary Fibrosis through KC-Mediated Neutrophil Chemotaxis

“…Since alveolar macrophage is the major source of pro-inflammatory chemokines upon phagocytosis of urban air particles [20], we then examined whether macrophage was activated by PM to secrete KC in bleomycin-induced pulmonary fibrosis. Immunofluorescence revealed the number of cells co-expression of KC and F4/80, a major marker of macrophages [21], on day 2-lung sections was significantly greater in the Bleo+PM group than in the control group ( Figure 4E). These data suggest that KC released by macrophage upon PM activation recruits neutrophils in bleomycin-induced pulmonary fibrosis.…”

EZH2 enhances expression of CCL5 to promote recruitment of macrophages and invasion in lung cancer

“…These results indicated that EZH2 overexpression promoted the macrophage recruitment, cell migration, and invasion via upregulating the expression of CCL5 in lung cancer cells. The in vivo subcutaneous xenotransplanted tumor model further confirmed that EZH2 knockdown inhibited lung cancer metastasis and macrophage recruitment, indicated by downregulation of molecular macrophage marker, F4/80 [ 35]. Meanwhile, the protein secretion of CCL5 was also inhibited by EZH2.…”