Three structurally related tyrosine receptor cell surface kinases, Tyro3, Axl, and Mertk (TAM) have been recognized to modulate immune function, tissue homeostasis, cardiovasculature, and cancer. The TAM receptor family appears to operate in adult mammals across multiple cell types, suggesting both widespread and specific regulation of cell functions and immune niches. TAM family members regulate tissue homeostasis by monitoring the presence of phosphatidylserine expressed on stressed or apoptotic cells. The detection of phosphatidylserine on apoptotic cells requires intermediary molecules that opsonize the dying cells and tether them to TAM receptors on phagocytes. This complex promotes the engulfment of apoptotic cells, also known as efferocytosis, that leads to the resolution of inflammation and tissue healing. The immune mechanisms dictating these processes appear to fall upon specific family members or may involve a complex of different receptors acting cooperatively to resolve and repair damaged tissues. Here, we focus on the role of TAM receptors in triggering efferocytosis and its consequences in the regulation of immune responses in the context of inflammation and cancer.

三种结构相关的酪氨酸受体细胞表面激酶 Tyro3、Axl 和 Mertk (TAM) 已被认为可调节免疫功能、组织稳态、心血管系统和癌症。TAM 受体家族似乎在多种细胞类型的成年哺乳动物中起作用，表明细胞功能和免疫微环境的广泛和特异性调节。TAM 家族成员通过监测应激或凋亡细胞上表达的磷脂酰丝氨酸的存在来调节组织稳态。检测凋亡细胞上的磷脂酰丝氨酸需要中间分子来调理垂死的细胞并将它们束缚在吞噬细胞上的 TAM 受体上。这种复合物促进凋亡细胞的吞噬，也称为细胞增多症，从而导致炎症消退和组织愈合。决定这些过程的免疫机制似乎落在特定的家族成员身上，或者可能涉及不同受体的复合体，它们协同作用以解决和修复受损组织。在这里，我们专注于 TAM 受体在触发细胞增多症中的作用及其在炎症和癌症背景下调节免疫反应的后果。