Abstract
Abstract Macrophages play a vital role in maintaining tissue homeostasis and defending against infections and cancer. Brown adipose tissue (BAT) is essential for expending surplus energy during cold stress, while white adipose tissue functions as the primary energy reservoir. The sympathetic nervous system responds to cold stress by releasing norepinephrine (NE), activating BAT through β3-adrenergic receptor. BAT-infiltrated macrophages exert opposing effects on thermogenesis, regulating the interplay between BAT cells and sympathetic nerves to either inhibit thermogenesis by clearing NE or enhance it by supporting sympathetic innervation of BAT. In mouse interscapular BAT, we identified a novel subset of CD3+ macrophages (CD45+ CD3+ CD4+ CD8+ CD11b+ F4/80+), whose frequency increased with chronic adrenergic stimulation. Despite the potential for T cell-monocyte doublets in flow cytometry, CD3+ macrophages demonstrated a unique surface expression pattern, lacking T cell markers CD62L and TCRβ. Furthermore, they showed elevated levels of Ly6C, MHCII, F4/80, and CD11b compared to T cells and CD3- macrophages. CD3+ macrophages exhibit heterogeneity in MHCII expression, with subsets expressing low and high levels. Since MHCII-expressing macrophages play a crucial role in regulating sympathetic nerve-BAT interaction, further characterization of CD3+ macrophages is pivotal for understanding the intricate mechanisms that govern adaptive thermogenesis regulation.
Published Version
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