Resilience of dermis resident macrophages to inflammatory challenges

Abstract

The skin serves as a complex barrier organ populated by tissue-resident macrophages (TRMs), which play critical roles in defense, homeostasis, and tissue repair. This review examines the functions of dermis resident TRMs in different inflammatory settings, their embryonic origins, and their long-term self-renewal capabilities. We highlight the M2-like phenotype of dermal TRMs and their specialized functions in perivascular and perineuronal niches. Their interactions with type 2 immune cells, autocrine cytokines such as IL-10, and their phagocytic clearance of apoptotic cells have been explored as mechanisms for M2-like dermal TRM self-maintenance and function. In conclusion, we address the need to bridge murine models with human studies, with the possibility of targeting TRMs to promote skin immunity or restrain cutaneous pathology. Our skin is more than just a physical shield; it’s a complex immune organ, filled with specialized cells like macrophages. In a detailed review, researchers explore these macrophages, focusing on their adaptability and function maintenance in the skin. This study synthesizes findings how macrophages interact with other immune cells, respond to inflammatory triggers, and contribute to tissue repair and homeostasis. The findings show that these macrophages can remain anti-inflammatory, even when faced with infections that usually trigger a strong immune response. They achieve this through various mechanisms, including interactions with specific immune cells that support their anti-inflammatory state, and engaging in processes that promote tissue repair without increasing inflammation. The researchers conclude that understanding these mechanisms opens new possibilities for treating skin diseases by targeting or mimicking the ways these macrophages control inflammation and support healing. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.