Exploring the versatile roles of tissue macrophages beyond immune defense

By Tarun Sai LomteApr 17 2024Reviewed by Lily Ramsey, LLM A recent study published in Science Immunology summarized the role of resident tissue macrophages in homeostasis and disease.

Recently, exploring RTM subsets to functional, developmental, and spatial levels has become feasible, helping identify mechanisms of tissue homeostasis. However, inflammation or disease markedly impacts their differentiation. During such disturbance, the differentiation of HSC-derived monocytes skews toward pro-reparative, tumor-supportive, or pro-inflammatory phenotypes, differing from that of steady-state RTMs.

Coexistence of RTM subsets within tissues Historically, it has been believed that organs and tissues are populated by unique tissue-specific RTMs during homeostasis, such as Langerhans cells in the skin, alveolar macrophages in the lungs, Kupffer cells in the liver, and microglia in the brain. Of the conserved PVM subsets, T cell immunoglobulin and mucin domain containing 4 PVMs emerge during embryogenesis in multiple organs and are characterized by low levels of major histocompatibility complex II and high levels of TIM4, folate receptor beta , lymphatic vessel endothelial hyaluronan receptor 1 , and cluster of differentiation 206 .

Microglia secrete growth factors critical for synapse formation. Additionally, they survey the brain microenvironment and modulate neuronal activity through synaptic engulfment and pruning. Besides, lung TIM4+ PVMs may be involved in wound healing, while the MHCII+ counterparts may be involved in antigen presentation and immune activation.

RTM dysregulation and disease It is established that HSC-derived iMacs are linked to chronic inflammatory diseases. This chronicity is thought to be due to ongoing inflammation leading to tissue function loss. Likewise, dysregulation of heart TIM4+ PVMs exacerbates fibrosis following cardiac infarction. Loss of RTM’s core homeostatic functions may impact cancer development.

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