Cytokines are a diverse group of low-molecular-weight, soluble proteins and glycoproteins that serve as critical mediators of immune and inflammatory responses¹. Produced predominantly by immune cells, these molecules orchestrate immune cell proliferation, differentiation, and functional modulation, thereby maintaining immune homeostasis and facilitating efficient pathogen defense mechanisms. The cytokine signaling circuit comprises numerous checkpoints that are often associated with feedback inhibition². This process helps the tissues to be in the non-inflammatory quiescent state of immunotolerance.

The diagnostic and prognostic value of cytokines in clinical practice is increasingly recognized, as their quantification in biological fluids provides insight into the immunological status and disease trajectory. Dysregulated cytokine production, such as in cytokine release syndrome (CRS), can precipitate life-threatening sequelae, including systemic inflammatory response syndrome (SIRS), multi-organ dysfunction, and mortality, as observed in severe cases of COVID-19⁴.

Cytokines can be broadly classified into type I and type II families. Type I cytokines predominantly mediate pro-inflammatory, cell-mediated immune responses, effectively targeting intracellular pathogens, particularly viruses^{5, 6}. In contrast, type II cytokines drive anti-inflammatory, humoral immune responses, essential for countering extracellular pathogens and modulating allergic and tissue repair processes⁶.

Key categories of cytokines

The key categories of cytokines include  interleukins(ILs),  interferons(IFNs), tumor necrosis factors (TNFs), colony-stimulating factors (CSFs), transforming growth factors (TGFs), and chemokines1. Additionally, proinflammatory cytokines promote inflammation, whereas anti-inflammatory cytokines help control and resolve inflammation to prevent excessive tissue damage.

Interleukins

ILs are key communicators between immune and non-immune cells, playing an important role in cancer development, progression, and control. They shape the tumor microenvironment by either promoting cancer growth or activating immune responses against tumors⁷. These dual properties of ILs present opportunities to improve advanced immunotherapies⁸, improving their effectiveness while minimizing side effects. IL-2 is being researched to be included in combination therapies for cancer treatment⁹.

Interferons

IFNs are key components of the innate immune response¹⁰. Pathogen invasion causes rapid activation of IFNs in most cells. IFNs are released by infected cells and initiate antiviral responses by acting on both neighboring and the same cells through paracrine and autocrine signaling pathways¹¹. IFNs play a significant role in the inflammatory innate response by activating IFN-stimulated genes (ISGs), which help establish an antiviral defense¹². IFNs play a vital role in controlling viral infections. For example, type III IFNs can successfully control the SARS-CoV-2 infection in intestinal epithelial cells¹³.

Tumor necrosis factors

TNF is vital for mounting an acute immune response, playing a key role in inflammation, fever, and sepsis. It promotes vasodilation, increases vascular permeability, and helps recruit immune cells such as neutrophils to sites of inflammation by regulating chemokine release and cell adhesion molecules^{14, 15}. Elevated levels of TNF-α are associated with the development of several autoimmune and inflammatory disorders, including rheumatoid arthritis, psoriasis, and inflammatory bowel disease¹⁶. Monoclonal antibodies targeting TNFs are used to treat these conditions¹⁷.

Colony-stimulating factors

CSFs are cytokines essential for the production and maturation of granulocytes and macrophages, playing significant roles in cancer progression¹⁸. In various cancers, CSFs such as granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and macrophage colony-stimulating factor (M-CSF) exert both pro- and anti-tumorigenic effects, influencing the tumor microenvironment^{19, 20, 21}. CSFs are being explored as potential adjuvant therapies in cancer treatment. For example, the use of GM-CSF as an adjuvant enhances humoral and cellular immune responses²².

Transforming growth factors

Transforming growth factor-beta (TGF-β) plays a key role in controlling immune function, cell proliferation, and differentiation. In cancer, TGF-β plays a dual role, it inhibits cell proliferation resulting in tumor suppression during early stages; however, during later stages of the disease, TGF-β promotes tumor progression by enhancing  epithelial-mesenchymal transition(EMT), immune evasion, and metastasis^{23, 24, 25}. TGF-β is a key target for therapeutic intervention. It plays an important role in immune system regulation, with mice lacking TGF-β1 showing severe multi-organ inflammation and early death²⁶.

Chemokines

Chemokines regulate chemotaxis and cell migration²⁷, directing immune cells to target sites, including those involved in immune surveillance. In addition to their role in immunity, chemokines contribute to embryonic development, angiogenesis, leukocyte recruitment, and tissue differentiation²⁷. Cells release chemokines in response to proinflammatory cytokines such as TNFs, IL-6, and IL-1β, playing a key role in the inflammatory response²⁷.

Cytokine function during immune response

Advances in cytokine and receptor engineering aim to modulate cytokine activity for therapeutic purposes²⁸, such as creating IL-2 variants to treat autoimmune diseases or enhance antitumor responses.

These strategies include altering receptor affinities, extending cytokine half-lives, and fine-tuning actions, with ongoing efforts to develop improved therapies for various diseases²⁹.

General functions of cytokines

Some of the key functions are listed below:

• Immune cell communication: Cytokines act locally through specific receptors in an autocrine, juxtacrine, or paracrine manner, modulating immune responses. For example, IL-1 facilitates interactions between lymphocytes to mount an effective adaptive immune response³⁰, acting as an important cell communication protein.
• Regulation of inflammation: Proinflammatory cytokines initiate inflammation to combat infection or heal tissue damage³¹. Conversely, anti-inflammatory cytokines help resolve inflammation to prevent excessive tissue damage³². Additionally, chemokines recruit and activate immune and inflammatory cells to sites of damage, highlighting their diverse roles in immune regulation and cell proliferation.
• Cellular differentiation and proliferation: Cytokines guide immune cell development and differentiation. The differentiation of naïve CD4+ T cells into T helper 2 (Th2) cells, the regulation of Th2 cytokine expression, and the signaling pathways involved play an important role in the immune response³³. Moreover, understanding type 2 immunity requires exploring the interconnected roles of Th2 cells, T follicular helper (Tfh) cells, and type 2 innate lymphoid cells (ILC2s)³⁴.
• Cytotoxicity and antimicrobial effects: Cytokines such as IFNs enhance the ability of immune cells to kill infected or malignant cells. For example, IFN-γ activates macrophages, boosting their antimicrobial capacity³⁵.
• Tissue repair and homeostasis: Beyond immune defense, cytokines such as TGF-β promote wound healing, tissue remodeling, and the maintenance of tissue homeostasis³⁶.
• Fever induction and reduction: Cytokines regulate and influence fever, with some acting as pyrogens, while others acting as antipyretics^{37, 38}. Key cytokines such as IL-1 and IL-6 play a central role in fever induction. TNF-α and IL-10 act as antipyretics, with TNF inhibition sometimes enhancing fever. Additionally, cytokines are involved in pain modulation³⁹, as their actions can affect the perception and intensity of pain during inflammatory responses.

Signaling pathways and mechanisms

Cytokines exert their biological effects through complex intracellular signaling pathways following the binding to specific cell-surface receptors. Cell signaling proteins and peptides actively transmit intercellular messages via autocrine or paracrine mechanisms, simultaneously modulating gene expression and cellular responses.

The primary signaling mechanisms of cytokines include:

JAK/STAT pathway

The binding of a cytokine to its receptors activates associated Janus kinases (JAKs), which in turn phosphorylate signal transducer and activator of transcription (STAT) proteins⁴⁰. The phosphorylated STATs dimerize and translocate to the nucleus to regulate gene expression⁴¹.

The pathway is a rapid and evolutionarily conserved signaling mechanism. It transmits extracellular signals to the nucleus in order to regulate vital processes in cancer, inflammation, and immune function. For example, the JAK-STAT pathway is central to the signaling of type I cytokines such as IL-2^{40, 41}, which modulate T cell proliferation and function.

Dysregulation of the JAK-STAT pathway is linked to various cancers and autoimmune diseases⁴¹, and research is advancing our understanding of its composition, activation, regulation, and potential as a therapeutic target.

MAPK pathway

Mitogen-activated protein kinase (MAPK) signaling plays an important role in regulating the production of cytokines in response to stimuli⁴². The pathway involves a cascade of kinases, including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38, which are activated in response to extracellular signals such as cytokines, growth factors, or stress⁴³.

These kinases activate downstream transcription factors that regulate gene expression, leading to the production of proinflammatory cytokines such as TNFs, IL-1, and IL-6. MAPK signaling is essential for coordinating immune responses, inflammation, and cellular stress responses, and dysregulation can contribute to various diseases such as autoimmune disorders and cancer⁴⁴.

Targeting specific components of the MAPK pathway offers potential therapeutic approaches to modulate cytokine production and manage related diseases⁴⁵.

PI3K-Akt pathway

The  phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathwayplays a significant role in regulating cytokine production and cellular responses in the brain, influencing immune cell activation, survival, proliferation, and apoptosis⁴⁶.

Activation of PI3K leads to the generation of phosphatidylinositol (3,4,5)-trisphosphate (PIP3). PIP3 activates AKT⁴⁷, a key regulator of various downstream signaling molecules such as mechanistic (or mammalian) target of rapamycin (mTOR), and Forkhead box O (FOXOs). The PI3K/AKT pathway plays a protective role in neuroinflammation and neurodegenerative diseases⁴⁸.

Dysregulation of the PI3K-Akt pathway has been linked to psychiatric disorders such as depression, where it affects cytokine balance and immune system function⁴⁹. This suggests that targeting the PI3K/Akt pathway may offer therapeutic strategies for both neurological and mood disorders.

Cytokine receptors and signaling

Cytokine receptors are classified into several groups based on their structural motifs and function ⁴⁰. They consist of multiple protein chains with extracellular regions containing a hemopoietin domain formed by Fibronectin type III domains⁵⁰, where the principal binding site for cytokines is located at the junction of these domains.

Cytokine receptors can be broadly categorized into six principal families: type I cytokine receptors, type II cytokine receptors, TNF receptor family, IL-1 receptor family, tyrosine kinase-associated receptors, and chemokine receptors⁵¹.

Class I cytokine receptors (Type I receptors)

Class I cytokine receptors are membrane proteins containing four α-helices, with their N terminus on the extracellular side and C terminus on the intracellular side. The N terminus interacts with ligands and initiates signaling cascades. These receptors either possess intrinsic kinase activity or contain adapter domains that interact with kinases, triggering downstream signaling. Class I receptors interact with IL, growth factors, and hematopoietins⁴⁰. Cytokine receptors such as gp130 and IL-4R are associated with JAKs for signaling⁴⁰.

Class II cytokine receptors (Type II receptors)

Class II cytokine receptors bind IFNS (α, β, γ, λ, ε, κ, and ω) and IL-10 family cytokines⁴⁰. The receptor signaling involves heterodimeric receptor complexes that bind one molecule of cytokine to initiate the cascade. These receptors typically bind to JAKs.

TNF receptor superfamily

This diverse group of receptors binds TNF-related cytokines and plays roles in apoptosis, inflammation, and immune regulation⁵². Many of these receptors possess intracellular death domains (DD) that initiate caspase cascades⁵². For example, the Fas receptor (CD95), upon binding to the Fas ligand, induces apoptosis in target cells⁵². It is an important mechanism for maintaining immune homeostasis and eliminating autoreactive lymphocytes.

IL-1 receptor family

These receptors recognize members of the IL-1 family. They share structural features with immunoglobulins,signaling through myeloid differentiation primary response 88 (MyD88) and IL-1 receptor-associated kinase (IRAK), leading to NF-κB activation and proinflammatory gene expression^{53, 54}. The IL-1 receptor is a key mediator of fever and inflammation during infections.

Chemokine receptors

Chemokine receptors are G protein-coupled receptors (GPCRs) that mediate leukocyte chemotaxis and positioning within tissues⁵⁵. Upon ligand binding, they activate intracellular signaling cascades that direct cell migration. CXCR4, a receptor for the chemokine CXCL12, is vital for hematopoietic stem-cell homing to the bone marrow⁵⁶.

Inflammatory cytokines

Inflammatory cytokines are secreted by immune cells, with some promoting inflammation and others reducing it³¹. These cytokines regulate each other, and imbalances in their activity can contribute to the development of diseases such as major depressive disorder, bipolar disorder, and schizophrenia^{57, 58}. Maintaining the balance between pro- and anti-inflammatory cytokines is important for healthy immune and systemic function.

Proinflammatory cytokines

Proinflammatory cytokines play key roles in driving inflammation, immune responses, and tissue destruction during infection or trauma⁵⁸. Proinflammatory cytokines can cause severe effects such as fever, inflammation, and even shock, underscoring the importance of regulating their activity. Examples include IL-1β, IL-2, IL-8, TNF-alpha, and IFN-γ.

Pathological association

• Autoimmune diseases are driven by the immune system’s misidentification of self-antigens, often worsened by proinflammatory molecules that promote chronic inflammation and autoimmune responses through effects on innate and adaptive immune cells⁵⁹. Targeting these proinflammatory cytokines has emerged as a promising therapeutic strategy to reduce inflammation and manage the progression of autoimmune diseases⁵⁹.
• Cytokines such as IL-23 and IL-17 drive the immune-mediated inflammation in psoriasis by disrupting skin barrier functions and promoting chronic immune activation⁶⁰. While therapies targeting these cytokines have shown superior efficacy in psoriasis, their precise mechanisms and interplay with genetic and environmental factors remain areas of active research, emphasizing the need for more personalized and targeted treatment approaches.

Anti-inflammatory cytokines

Anti-inflammatory cytokines are immunoregulatory molecules that help control the proinflammatory cytokine response and regulate the immune system messengers⁶¹. They work alongside cytokine inhibitors and soluble cytokine receptors to modulate inflammation. Examples include IL-1 receptor antagonist, IL-4, IL-6, IL-10, IL-11, and IL-13.

Pathological association

Asthma is a chronic airway inflammatory disease driven by IL-4, IL-5, and IL-13, which cause eosinophilia, mucus overproduction, and bronchial hyperresponsiveness⁶². Understanding the diverse cytokine networks and heterogeneity of asthma is vital for developing targeted therapies to address the spectrum of disease mechanisms.

Below is a list of proinflammatory and anti-inflammatory cytokines with their source and functions.

Proinflammatory cytokines

Anti-inflammatory cytokines

Cytokine dysregulation and disease

Cytokines regulate immune and inflammatory responses, maintaining the balance between proinflammatory and anti-inflammatory signals to ensure homeostasis⁷⁹. Dysregulation of this balance is implicated in various diseases, including autoimmune disorders, allergies, chronic infections, atherosclerosis, major depression, obesity, and metabolic syndrome.

The dysfunction can result from abnormalities in the neuroendocrine-immune interface, leading to persistent inflammation and a failure to resolve it, which negatively impacts overall health, behavior, quality of life, and metabolic and cardiovascular health.

Cytokine storm and its implications

Cytokine storm, or cytokine release syndrome (CRS) in severe COVID-19 cases results from a dysregulated immune response, marked by delayed production of type-I and type-III IFNs and a subsequent surge in proinflammatory cytokines such as IL-6, IL-8, and TNFα⁸⁰. This uncontrolled inflammatory response causes macrophage and neutrophil infiltration, leading to lung injury and worsening disease severity⁸¹.

Cytokine storm-like syndromes can also cause severe tissue damage, including lymphocyte dysfunction, vascular barrier damage, multi-organ failure, and potentially death⁸².

Role in chronic inflammation

Cytokines are key drivers of chronic inflammation, mediating immune responses that contribute to the progression of Alzheimer’s disease, atherosclerosis, and type II diabetes⁸³. Proinflammatory cytokines such as IL-6, TNF-α, and IL-1β are elevated in chronic inflammatory states, signifying tissue damage and dysregulated immune activation⁸⁴.

Understanding the role of cytokines in chronic inflammation is important for developing targeted therapies to mitigate their harmful effects and slow the progression of inflammatory diseases.

Impact on cancer progression

Cytokines play an important role in cancer progression by promoting tumor initiation, growth, metastasis, angiogenesis, and therapeutic resistance within the tumor microenvironment (TME)⁸⁵. Chronic inflammation and infection contribute to the TME, exacerbating cancer symptoms such as pain, fatigue, and cachexia while also reducing patients’ quality of life.

ILs, IFNs, and growth factors influence tumor growth, TME, and treatment outcomes⁸⁶. Targeting cytokine pathways offers effective strategies to modulate immunity, inhibit tumor progression, and combat the immunosuppression seen in advanced cancer.

T cell cytokines and immunity

T lymphocytes are key players in cellular immunity, producing cytokines to mediate inflammation and regulate other immune cells⁸⁷. CD4⁺ T cells have diverse subsets, each with distinct roles in immunity and immune-related diseases, alongside other T cell types⁸⁷. Understanding the regulation and function of cytokines has played a vital role in developing innovative treatments for various diseases.

Cytokines produced by T cells

The T helper cell marker CD4⁺ regulates adaptive immunity by promoting inflammation and antibody production. On the basis of cytokine secretion, they are categorized as Th1, Th2, and Th17 cells.

• Th1 cells produce IFN-γ to enhance cellular immunity by activating macrophages⁸⁷. These cells are vital for combating intracellular pathogen defense mechanisms.
• Th2 cells secrete IL-4, IL-5, and IL-13 to support humoral immunity and B cell proliferation⁸⁷. These cells focus on controlling extracellular pathogens. IL-13 also aids in primary antibody production.
• In contrast, Th17 cells are central to autoimmune disease progression, with their development and function uniquely regulated by IL-23⁸⁷.
• T regulatory cells (Treg1) primarily produce IL-10 and IFN-γ, along with small amounts of IL-5 and TGF-β⁸⁸. Treg3 cells mainly produce high levels of TGF-β and small amounts of IL-10⁸⁹.

Role in T-cell activation and differentiation

The activation and differentiation of CD4⁺ T cells is influenced by T cell receptor signaling⁸⁷, costimulatory receptors, and cytokines produced during innate immune responses, which signal the nature of infections or environmental stimuli.

• IL-12 promotes Th1 differentiation by upregulating IL-12Rβ2 on Th1 cells, ensuring their propagation and maintenance⁸⁷.
• IL-33, an alarmin cytokine produced by epithelial cells, enhances Th2 differentiation by activating its receptor ST2, which boosts the production of IL-5 and IL-13, contributing to allergic inflammation⁸⁷.
• Similarly, IL-25, produced by tuft and airway brush cells in response to allergens, supports Th2 differentiation and function by engaging the IL-17RA/IL-17RB receptor complex and increasing IL-4 production⁸⁷.

Measuring cytokine levels

Quantifying cytokine levels is critical for investigating immune responses and inflammation¹. Various body fluids can be used for cytokine measurement, with blood, specifically serum or plasma, being the most common owing to its ability to reflect the immune status of the body.

Cytokines have short half-lives and are prone to degradation, making proper sample collection and handling essential to avoid false-negative results¹. Serum derived from clotted blood may show elevated cytokine levels due to release during clot formation, while plasma, obtained using anticoagulants such as EDTA, better preserves cytokine stability.

Anticoagulants such as heparin can induce cytokine release from blood cells, affecting measurements, with EDTA plasma showing the most consistent results compared with heparin or citrate-treated samples¹. Rapid processing of blood samples is recommended to ensure accurate cytokine quantification and minimize time-dependent changes.

Techniques and assays for measuring cytokines

Most cytokine detection methods are antibody-based immunoassays, such as enzyme-linked immunosorbent assay (ELISA) and cytometric bead array (CBA)⁹⁰. Mass spectrometry methods directly measure analytes. Among the various methods, electrochemiluminescence assays are known for their high sensitivity and dynamic range, although they involve a non-homogeneous process. In contrast, CBA offers robust sensitivity, versatility, and the ability to detect multiple cytokines simultaneously using a homogeneous process.

ELISA is a widely used, cost-effective method offering specificity and sensitivity for cytokine analysis. The indirect sandwich ELISA format enables accurate cytokine detection and quantification, and sequential ELISA assays can be used to analyze multiple cytokines from small sample volumes. Multiplex ELISA allows for the simultaneous detection of various cytokines, though it requires careful consideration of factors such as cost and assay development time.

Importance in diagnostics

Because cytokines exert complex, sometimes even opposing and synergistic effects, measuring their levels has become vital in clinical diagnostics for evaluating immunologic, inflammatory, and infectious diseases⁹¹.

Cytokine profiling is simpler and more cost-effective than genetic testing, and plays an essential role in diagnosing diseases with unclear etiologies⁹². Furthermore, cytokine assessments help guide treatment decisions, particularly in identifying targeted biologic therapies that reduce the need for trial-and-error approaches while minimizing potential side effects.

Cytokine profiling is also indispensable in drug discovery, serving as a tool for identifying disease biomarkers and screening potential drug candidates. Technologies used in cytokine profiling must exhibit sensitivity, robustness, multiplexing capabilities, and high-throughput potential⁹⁰.

Recombinant cytokines

Recombinant cytokines have proven valuable in treating various diseases, addressing toxicities associated with pharmacological immunostimulators that can disrupt natural cytokine regulation⁹³.

Definition of recombinant cytokines

Recombinant cytokines are engineered to stimulate specific immune cells or general immune responses, especially when the body faces immunosuppressive signals from pathogens or tumors⁹³. The production of recombinant human cytokines as therapeutic proteins is important for medical treatments, requiring the development of suitable host cells and expression systems.

Advances in recombinant cytokine research

Recombinant cytokines were initially produced using Escherichia coli, but the lack of post-translational modifications (PTMs) in this system led to a preference for eukaryotic hosts, such as yeast, animal, plant, and insect cells. Although E. coli cells can also be modified to introduce certain PTMs such as glycosylation, eukaryotic systems such as yeast, animal, plant, and insect cells are currently used for further advancements.

Advances in genetic and metabolic engineering have significantly improved the efficiency of recombinant cytokine production. Further bioprocess optimizations, such as enhancing cell culture conditions and selecting appropriate bioreactors, are expected to improve large-scale production.

Future directions in cytokine research

Cytokine research has evolved from studying their functional activities in tissue cultures to investigating their molecular structures and receptor interactions. This area of study, known as cytokinology is now a specialized discipline that involves expertise in cytokine assays, signal transduction, gene activation, along with therapeutic applications of cytokine agonists and antagonists⁹⁴.

Recent advancements have led to the identification of novel cytokines and their roles in various biological processes, demonstrating therapeutic success, particularly with cytokine inhibitors. This progress suggests that the study of cytokines may become an independent field within immunology and medicine.

Emerging trends and technologies

Emerging trends, such as protein engineering, structure-based designs, directed evolution, and computational tools, have accelerated the development of novel cytokine mimetics and improved the pharmacokinetics and pharmacodynamics of existing cytokine therapies⁹⁵.

A notable example is Neoleukin-2/15 (Neo-2/15), a de novo engineered cytokine with enhanced stability and efficacy in cancer treatment, demonstrating the growing potential of computationally designed cytokine therapeutics⁹⁵.

The potential of cytokines in disease management

Over the past 40 years, cytokines and their receptors have been studied as potential cancer treatments, with strategies aimed at enhancing the growth-inhibitory and immunostimulatory effects of certain cytokines or inhibiting those promoting inflammation and tumor growth.

Despite promising preclinical results, clinical trials involving cytokines or cytokine antagonists show limited therapeutic efficacy⁸⁶, often owing to the advanced stage of the diseases in the trials. New approaches are focusing on combining cytokine-based therapies with other treatments to improve efficacy, especially for early-stage cancers, by a better understanding of the tumor microenvironment⁹⁶. However, challenges remain in delivery methods and the complex roles of cytokines.

Conclusion

Cytokines are essential regulators of immune responses and inflammation, with significant implications for disease progression, diagnosis, and therapy. Advancements in cytokine research have provided deeper insights into their diverse roles, from promoting tissue repair to exacerbating chronic inflammation and cancer progression.

The development of recombinant cytokines and inhibitors holds promise for managing autoimmune diseases, infections, and cancer. Continued innovations in protein engineering and cytokine profiling technologies are paving the way for more targeted and effective treatments. As research in this area progresses, cytokines are poised to transform disease management and play a central role in future immunological therapies.

FAQs

How do cytokines contribute to inflammatory responses?

Cytokines modulate inflammatory responses by signaling and regulating immune cells to initiate and sustain inflammation. Proinflammatory cytokines promote inflammation by activating immune cells, increasing vascular permeability, and recruiting other immune cells to sites of infection or injury. Anti-inflammatory cytokines resolve inflammation by suppressing the activity of proinflammatory cytokines, maintaining balance, and preventing excessive tissue damage.

How do recombinant cytokines differ from naturally occurring cytokines?

Recombinant cytokines are lab-made versions of naturally occurring cytokines produced through genetic engineering in organisms such as bacteria or mammalian cells. Unlike natural cytokines, which the body produces in response to infection or injury, recombinant cytokines are designed for controlled production and therapeutic use. They are often modified for enhanced stability, activity, or reduced immune reactions and are used in treatments for conditions such as cancer and autoimmune diseases.

How do cytokines influence the development of diseases such as cancer and atherosclerosis?

Cytokines influence the development of diseases such as cancer and atherosclerosis by regulating inflammation and immune responses. In cancer, certain cytokines promote tumor growth, metastasis, and immune evasion, while others may help combat tumor cells. In atherosclerosis, proinflammatory cytokines contribute to plaque formation, endothelial dysfunction, and the progression of arterial disease. Dysregulated cytokine activity in both conditions can drive chronic inflammation, which worsens disease progression and complications.

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