IL1B
Interleukin 1 Beta
Gene Number: 3553
Location: 2q14
Key Functions: Pro-inflammatory signaling, fever induction, immune system activation
The IL1B gene, located on chromosome 2q14, encodes interleukin-1 beta (IL-1β), one of the most powerful mediators of inflammation in the human body. As a member of the interleukin-1 cytokine family, IL-1β serves as a key molecular signal linking innate immune activation to systemic inflammatory responses such as fever, leukocyte recruitment, and acute-phase protein synthesis.
IL-1β is initially synthesized as pro–IL-1β, an inactive cytosolic precursor requiring proteolytic cleavage by caspase-1 to become active. This activation occurs within the inflammasome complex, most commonly the NLRP3 inflammasome, which acts as the molecular gatekeeper of IL-1β maturation.
Upon activation, mature IL-1β is secreted and binds to the IL-1 receptor (IL-1R1) on target cells, triggering intracellular signaling through MyD88 and NF-κB pathways. The result is the transcription of numerous inflammatory genes—amplifying cytokine release, inducing fever via the hypothalamus, and promoting endothelial activation to facilitate immune cell migration.
From a genetic perspective, IL1B polymorphisms significantly influence an individual’s inflammatory tone and disease susceptibility. Variants such as rs16944 (-511C>T) and rs1143634 (+3954C>T) are known to modulate IL-1β production, with the high-expression alleles linked to increased risk of autoimmune diseases, atherosclerosis, type 2 diabetes, and cancer-related inflammation. Conversely, reduced IL-1β signaling may impair host defense against infection, illustrating the delicate evolutionary balance between protection and pathology.
Functionally, IL-1β sits at the crossroads of immune activation and systemic inflammation, integrating signals from damaged or infected tissues into coordinated physiological responses. While transient IL-1β activity is essential for pathogen clearance and tissue repair, chronic or dysregulated signaling contributes to persistent inflammatory states, driving rheumatoid arthritis, inflammatory bowel disease, neuroinflammation, and metabolic syndrome. Thus, IL1B represents both a vital defender and a potential instigator—its potency demanding tight regulation to preserve immune equilibrium.
SNP ID | Your Genotype | Alternative Alleles | Interpretation |
|---|---|---|---|
rs16944 | No matching variant or no valid DNA data | G | No interpretation available |
rs1143634 | No matching variant or no valid DNA data | A | No interpretation available |
rs16944
GG –Elevated IL-1β and LPS response; associated with increased cortisol resistance (R).
AG – Intermediate IL-1β activity; moderate inflammation risk (R).
AA –Lower IL-1β activity; associated with reduced inflammatory signaling (R).
Functional effect: The G allele upregulates IL-1β expression in response to immune triggers, enhancing pro-inflammatory signaling and increasing vulnerability to autoimmune and stress-related conditions.
rs1143634
AA – Highest IL-1β expression; increased pro-inflammatory signaling (R).
AG – Moderately increased IL-1β activity; associated with higher autoimmune and metabolic risk (R).
GG – Baseline IL-1β expression; typical inflammation profile (R).
Functional effect: The A allele enhances IL-1β transcription and cytokine release—elevating inflammatory response—but may confer context-dependent protection in certain acute conditions (R).
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