Интерлейкин 1 (РАИЛ-1)

Interleukin-1 beta (IL1B) C(+3953)T genetic variant testing, also described as IL‑1β C3953T or IL1B +3953 C>T, assesses a functional polymorphism associated with increased IL‑1β production and a more robust inflammatory response. The assay is used to evaluate genetic predisposition to inflammation-driven conditions, most notably severe periodontitis, and is also cited in studies of cardiovascular pathology. Results are interpreted in conjunction with clinical findings and other risk factors. Testing is often paired with IL1A C(−889)T to better characterize the inflammatory phenotype. The marker informs risk rather than diagnosing disease, and it does not have a “normal/pathologic” reference classification.

IL‑1 is a key cytokine family that orchestrates inflammatory and immune responses. IL‑1α and IL‑1β are proinflammatory mediators, whereas the IL‑1 receptor antagonist (IL‑1RN) tempers signaling; the corresponding genes are IL1A, IL1B, and IL1RN. These cytokines act at very low concentrations and are produced transiently in response to antigenic stimulation by cells such as activated macrophages, keratinocytes, stimulated B lymphocytes, and fibroblasts. The biological effects of IL‑1β are mediated through binding to the IL‑1RI membrane receptor. The IL1B C(+3953)T polymorphism represents a substitution of cytosine with thymine at position +3953. Genotypes include CC, CT, and TT. This variant is linked to differential gene expression: individuals with one T allele (CT) produce approximately twice as much IL‑1β as CC homozygotes, and TT homozygotes produce roughly fourfold higher amounts. Carriage of the T allele is therefore associated with a more intense inflammatory response. Clinically, the T allele has been associated with more acute and severe forms of periodontitis and with a tendency toward chronic disease persistence. A higher frequency of the T allele has also been reported among patients with osteomyelitis compared with population controls, and carriers of TT or CT genotypes have been observed to have lower body fat mass than CC homozygotes. Associations with cardiovascular pathology have been described. Because this is a gene polymorphism, there is no concept of “normal” or “pathologic” results; findings indicate inherited variation that may modify inflammatory risk. Testing is commonly considered alongside IL1A C(−889)T and may be included in panels that estimate genetic risk for periodontitis and its complications.