Harris Aziza, Patel Preeti
Cipto Mangunkusumo National Hospital, Jakarta, Indonesia
Interleukins (ILs) are a large family of cytokines that function as key mediators of immune cell communication, regulating cell proliferation, differentiation, motility, and survival across both innate and adaptive immunity. The term was first introduced in the late 1970s to describe leukocyte-derived cytokines, with IL-1 identified as a leukocytic pyrogen and IL-2 as a T-cell growth factor. Since then, more than 60 cytokines have been designated as interleukins, and to date, at least 38 have been formally recognized (IL-1 through IL-38). Interleukins are structurally diverse but are commonly grouped into families based on receptor usage, sequence homology, and biological function. Major families include the following: IL-1 family: IL-1α, IL-1β, IL-18, IL-33, IL-36, IL-37, and IL-38. Common γ-chain family: IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. IL-6/IL-12 family: IL-6, IL-11, IL-12, IL-23, and IL-27. IL-17 family: IL-17A through IL-17F and IL-25. Each family orchestrates specific pathways in host defense, inflammation, hematopoiesis, and tissue repair. From a historical perspective, IL-1 and its receptor antagonist (IL-1Ra) have become the prototypes for understanding the balance between pro- and anti-inflammatory cytokines. IL-2, initially described as a T-cell mitogen, was later shown to play a central role in immune regulation and tolerance. IL-10 emerged as a master anti-inflammatory cytokine, functioning as a key regulator in infection and autoimmunity. The discovery of T-helper (Th)17 cytokines, particularly IL-17 and IL-23, provided new insights into chronic inflammation and autoimmunity. Collectively, these discoveries established the conceptual framework that interleukins act not only as immune stimulators but also as immunoregulators. Clinically, interleukins have become both biomarkers and therapeutic targets. Dysregulated signaling is implicated in autoimmune diseases, such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis, as well as in malignancies, infections, and hyperinflammatory states, including cytokine storms. Therapeutic blockade of interleukin pathways, including anakinra (IL-1Ra), tocilizumab (IL-6 receptor blocker), and secukinumab (IL-17A inhibitor), has transformed management across rheumatology, dermatology, oncology, and infectious diseases.
白细胞介素（IL）是一类细胞因子，最初被认为仅由白细胞表达，但后来发现许多其他体细胞也能产生。它们在免疫细胞的激活和分化以及增殖、成熟、迁移和黏附中发挥着重要作用。它们还具有促炎和抗炎特性。因此，白细胞介素的主要功能是在炎症和免疫反应过程中调节生长、分化和激活。白细胞介素由一大类蛋白质组成，这些蛋白质通过与细胞表面的高亲和力受体结合，可在细胞和组织中引发多种反应。它们具有旁分泌和自分泌功能。白细胞介素也用于动物研究，以调查与临床医学相关的方面。细胞因子是针对病原体和其他抗原产生的蛋白质，可调节和介导炎症和免疫反应。白细胞介素的产生是一个自我限制的过程。编码大多数白细胞介素的信使核糖核酸不稳定，导致短暂合成。这些分子一旦合成便迅速分泌。细胞对白细胞介素的反应包括上调和下调机制，这是由编码细胞因子受体抑制剂的基因诱导和参与的。白细胞介素具有冗余功能。例如，IL-4、IL-5和IL-13是B细胞生长因子，可刺激B细胞分化。细胞因子刺激B细胞中抗体亚型的转换、辅助性T细胞分化为Th-1和Th-2亚群以及吞噬细胞中杀菌机制的激活。白细胞介素常常影响其他白细胞介素的合成和作用。例如，IL-1促进淋巴细胞激活，导致IL-2释放。细胞对细胞因子的反应受到外部信号或高亲和力受体的刺激和调节。例如，病原体对B细胞的刺激导致细胞因子受体表达增加。大多数细胞因子要么作用于分泌该细胞因子的同一细胞，例如，T细胞产生的IL-2作用于产生它的同一T细胞，要么作用于附近的细胞。此外，细胞因子可能进入循环并在远离产生部位的地方发挥作用，例如，IL-1是一种内源性热原，作用于中枢神经系统（CNS）并引起发热。占据受体并引发生物学效应只需少量的细胞因子。
