In the complex mechanisms by which the body defends against external threats and maintains internal homeostasis, interleukins (ILs), as core members of the cytokine family, play a crucial role as "signal commanders." These seemingly tiny protein molecules regulate the activation, proliferation, and differentiation of immune cells through precise signal transmission, maintaining the balance and efficiency of immune responses. From being initially recognized merely as "messengers between white blood cells" to now being confirmed to participate in multiple physiological processes such as hematopoiesis, inflammation, and tissue repair, research on interleukins has always led breakthroughs in the field of immunology, providing important support for understanding disease mechanisms and developing targeted therapies.
Interleukins are a class of small-molecule proteins secreted by immune cells and various tissue cells. They mediate intercellular communication and regulate biological effects by binding to receptors on the surface of target cells. Although the term retains "leukocyte," modern research has confirmed that their producing cells include various types such as T cells, macrophages, and endothelial cells, and their targets have expanded to hematopoietic stem cells, nerve cells, etc., with functions far beyond the initial definition.
In the 1970s, the immunology community fell into naming chaos due to the discovery of a large number of immune regulatory factors. In 1979, the Second International Symposium on Lymphokines established a unified naming rule: such factors involved in interactions between immune cells were collectively referred to as "interleukins," numbered sequentially with Arabic numerals (e.g., IL-1, IL-2). This standardization laid the foundation for systematic research, and currently, 35 members (IL-1 to IL-35) have been identified, forming a regulatory network with intertwined functions.
Interleukins exhibit significant characteristics of "one factor with multiple effects and multiple factors with the same effect": one factor can be produced by multiple cell types (e.g., IL-6 can come from T cells, macrophages, and endothelial cells); one factor can act on multiple target cells (e.g., IL-2 can simultaneously regulate T cell proliferation, NK cell activation, and B cell differentiation). This diversity enables the immune system to achieve complex regulation through a limited number of molecules.
As emergency signal molecules, interleukins have the characteristics of "rapid response and immediate clearance": they are rapidly synthesized and secreted upon stimulation, and degraded within minutes to hours after functioning, ensuring the timeliness of signals. Their mode of action is mainly local paracrine and autocrine (e.g., IL-8 at inflammatory sites), and a few exert systemic effects through the bloodstream (e.g., IL-6-mediated acute-phase response), achieving precise spatiotemporal regulation.
These molecules are mostly glycoproteins with a molecular weight of 10-30 kDa, and their concentration in the body is only at the pg/mL level, but they can trigger significant physiological responses through cascade amplification effects. For example, a small amount of IL-2 can initiate T cells to enter the proliferation cycle from a quiescent state, triggering specific immune responses. This high efficiency makes them ideal targets for immune regulation.
The IL-1 family (represented by IL-1β) is an "early warning signal" after infection or injury. It can activate vascular endothelial cells to express adhesion molecules, recruit neutrophils to gather at inflammatory sites, and act on the hypothalamus to cause fever, hence being called "endogenous pyrogens." IL-8, as a potent chemokine for neutrophils, guides immune cells to accurately reach the lesion in acute inflammation, enhancing phagocytic clearance ability.
IL-2 is the "engine" of T cell proliferation. It is produced by activated T cells in an autocrine manner, promoting them to enter the S phase from the G0 phase. It also induces the differentiation of cytotoxic T cells and enhances the killing activity of NK cells, being the core driver of specific immune responses. IL-4, mainly secreted by Th2 cells, promotes B cell proliferation, differentiation, and antibody class switching (e.g., to IgE), playing a leading role in humoral immunity and allergic reactions. IL-10 acts as an "immune brake," inhibiting Th1 cells from releasing pro-inflammatory factors and reducing the antigen-presenting ability of macrophages, avoiding tissue damage caused by excessive immune activation.
IL-3 (multipotent colony-stimulating factor) can stimulate the proliferation and differentiation of multipotent hematopoietic stem cells and various lineages of progenitor cells, providing sufficient "reserve forces" for the blood system. It is clinically expected to be used in the treatment of aplastic anemia. IL-11, secreted by bone marrow stromal cells, synergizes with thrombopoietin to promote the maturation of megakaryocytes, showing potential in the prevention and treatment of post-chemotherapy thrombocytopenia, and also participates in bone marrow tissue repair, accelerating the recovery of hematopoietic function.
IL-6 is a "bridge molecule" connecting immunity and inflammation. It not only promotes B cell differentiation and T cell activation but also induces the liver to synthesize acute-phase proteins. Its abnormal elevation is closely related to chronic inflammatory diseases such as rheumatoid arthritis and psoriasis. The IL-17 family (represented by IL-17A), secreted by Th17 cells, exacerbates chronic inflammation by inducing epithelial cells to release pro-inflammatory factors, being a core driver of autoimmune diseases such as psoriasis and ankylosing spondylitis. Currently, a variety of targeted drugs have been used clinically.
Interleukins play irreplaceable roles in immune defense, hematopoietic regulation, tissue repair, etc., through building a precise signal network. Their functional imbalance is a common mechanism of various diseases: excessive activation may trigger autoimmune diseases, while insufficient activity leads to immunodeficiency or tumor escape.
Currently, therapies targeting interleukins have achieved breakthroughs in clinical practice: anti-IL-6 receptor antibodies for rheumatoid arthritis, anti-IL-17 antibodies for improving psoriasis, and IL-2 receptor antagonists for anti-rejection in organ transplantation, etc. In the future, with the development of single-cell technology and structural biology, new functions, new receptors, and specific regulatory mechanisms of the interleukin family will be gradually revealed, providing more accurate targets for precise immunotherapy.
As "signal commanders" of the immune system, research on interleukins not only deepens human understanding of life regulation but also continuously promotes the innovation of disease treatment, offering infinite possibilities for deciphering the codes of immune-related diseases.
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