Phagocytosis is a pivotal immunological process, and its discovery by Elia Metchnikoff in 1882 was a step toward the establishment of the innate immune system as a separate branch of immunology. Elia Metchnikoff received the Nobel Prize in physiology and medicine for this discovery in 1908. Since its discovery almost 140 years before, phagocytosis remains the hot topic of research in immunology. The phagocytosis research has seen a great advancement since its first discovery. Functionally, phagocytosis is a simple immunological process required to engulf and remove pathogens, dead cells and tumor cells to maintain the immune homeostasis. However, mechanistically, it is a very complex process involving different mechanisms, induced and regulated by several pattern recognition receptors, soluble pattern recognition molecules, scavenger receptors (SRs) and opsonins. These mechanisms involve the formation of phagosomes, their maturation into phagolysosomes causing pathogen destruction or antigen synthesis to present them to major histocompatibility complex molecules for activating an adaptive immune response. Any defect in this mechanism may predispose the host to certain infections and inflammatory diseases (autoinflammatory and autoimmune diseases) along with immunodeficiency. The article is designed to discuss its mechanistic complexity at each level, varying from phagocytosis induction to phagolysosome resolution.

中文翻译：

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吞噬作用：在表型上简单而在机械上复杂的过程。

吞噬作用是关键的免疫学过程，它由Elia Metchnikoff在1882年发现，是朝着建立先天免疫系统作为免疫学的一个独立分支迈出的一步。Elia Metchnikoff于1908年因这项发现而获得了诺贝尔生理学和医学奖。自从其发现将近140年以来，吞噬作用一直是免疫学研究的热门话题。自从首次发现以来，吞噬作用研究已取得了巨大进步。从功能上讲，吞噬作用是吞噬和去除病原体，死细胞和肿瘤细胞以维持免疫稳态所需的简单免疫学过程。然而，从机制上讲，这是一个非常复杂的过程，涉及多种机制，由多种模式识别受体，可溶性模式识别分子，清道夫受体（SR）和调理素。这些机制涉及吞噬体的形成，它们成熟为吞噬体，引起病原体破坏或抗原合成，从而将它们呈现给主要的组织相容性复合物分子以激活适应性免疫应答。该机制的任何缺陷都可能使宿主易患某些感染和炎症性疾病（自身炎症性疾病和自身免疫性疾病）以及免疫缺陷。本文旨在讨论从吞噬作用诱导到吞噬溶酶体分解的每个水平的机制复杂性。它们成熟为吞噬溶酶体，引起病原体破坏或抗原合成，从而将它们呈递给主要的组织相容性复合物分子以激活适应性免疫反应。该机制的任何缺陷都可能使宿主易患某些感染和炎性疾病（自身炎症和自身免疫性疾病）以及免疫缺陷。本文旨在讨论从吞噬作用诱导到吞噬溶酶体分解的每个水平的机制复杂性。它们成熟为吞噬溶酶体，引起病原体破坏或抗原合成，从而将它们呈递给主要的组织相容性复合物分子以激活适应性免疫反应。该机制的任何缺陷都可能使宿主易患某些感染和炎症性疾病（自身炎症性疾病和自身免疫性疾病）以及免疫缺陷。本文旨在讨论其从吞噬作用诱导到吞噬溶酶体分解的各个阶段的机制复杂性。