Latest research on IL-1ra

Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001.

Latest findings

On the other hand, M2 macrophages are more predominant in SpA, late stage MS, and SS releasing anti-inflammatory cytokines such as IL-4, IL-10, IL-1ra, and TGF-β and contributing to tissue remodeling and angiogenesis. [source, 2016]
These processes are believed to be under the strict control of distinct regulatory mechanisms including the presence of a third biologically inactive subtype of IL-1, termed IL-1R antagonist (IL-1ra) [2, 18, 19]. [source, 2016]
IL-1ra binds to IL-1R1 with similar affinity to its biologically active counterparts, though binding fails to initiate downstream, intracellular signaling [20]. [source, 2016]
Several groups have found both IL-8 and interleukin 1 receptor antagonist (IL-1ra) to be significantly increased in CSF samples from patients with cerebral malaria compared to samples from those with severe malaria (Table 1) (148, 149). [source, 2016]
It is possible that IL-8 plays a role in recruiting the monocytes observed in pediatric patients, as well as enhancing angiogenesis (151), while IL-1ra could act to downregulate the inflammation response by directly competing with IL-1α and IL-1α receptor stimulation (153). [source, 2016]
Indeed, aging is associated with increased levels of TNF-α, IL-6, and interleukin-1 receptor agonist (IL-1ra) and systemic inflammatory biomarkers such as C-reactive protein (CRP) as well as higher count of inflammatory cells such as neutrophil and monocytes [151–153]. [source, 2016]
Physical activity/exercise also induces the release of several myokines from skeletal muscle such as IL-6 [210–212], which suppresses IL-1 and TNF-α [213] and triggers the release of many anti-inflammatory cytokines such as IL-1 receptor antagonist (IL-1ra) and IL-10, in addition to Cortisol [214, 215]. [source, 2016]
A panel of 13 proteins was shown to have significant differences in striatum samples between the disease groups by One-way ANOVA (Table 3)—CCL28 (C–C motif ligand 28 or mucosae-associated epithelial chemokine), HCC-1 (CCL-14), IL-18 binding protein a (IL-18BPa), PF4 (platelet factor 4), interferon-gamma (IFN-γ), IL-1 receptor antagonist (IL-1ra), IL-2, IL-15, PDGF-AA, PDGF-BB, TNF-α, Dtk (tyrosine-protein kinase receptor TYRO3), and ErbB3 (also HER3, human epidermal growth factor receptor 3). [source, 2016]
Proteins Dtk, ErBb3, IL-1ra, and IL-5 that had shown significant disease group differences in the antibody arrays for striatum showed significant correlations with tangle scores (Table 9, bold). [source, 2016]
In striatum, there were decreases in PD compared to control for PDGF-AA, PDGF-BB, ErbB3, Dtk, PF4 and HCC-1, IL-18BPa and CCL28, but increases in PD for cytokines IL-2, IFN-γ, TNF-α, IL-1ra, and IL-15. [source, 2016]