Sentence examples for release of interleukin-2 from inspiring English sources

(C) Release of interleukin-2 (IL-2).

Acute GVHD pathogenesis is a multi-step process, initiated in part by cytokine release from tissue damaged during cytotoxic preparative regimens, resulting in donor T-cell activation, and subsequent release of interleukin-2 (IL-2), tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ).

The lipid profile, fasting and 2-h post-glucose load plasma glucose levels, homeostasis model assessment index (HOMA), plasma high-sensitivity C-reactive protein (hsCRP) levels and lymphocyte release of interleukin-2, interferon-γ and tumor necrosis factor-α were assessed at baseline, on the day of randomization, and after 4 and 12 weeks of treatment.

Macrolides reduce the release of interleukin-8 and tumor necrosis factor-α, and the adherence of Streptococcus pneumoniae to respiratory epithelial cells.

Then, we designed scaffolds for bone regeneration based on modifications of decellularized bone for a short release of interferon-gamma (IFNg) to promote the M1 phenotype, followed by a more sustained release of interleukin-4 (IL4) to promote the M2 phenotype.

The enhanced release of interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-α) by the THP-1 macrophages suggested that the needle-shaped CaCO3 particles trigger a pro-inflammatory response.

To this end, a system of double hydrogel layers on titania nanotubes (TNT) was prepared as reservoir to modulate the release of interleukin-4 (IL-4) and interferon-γ (IFN-γ).

Alternative causes of this tissue damage have been proposed and involve release of interleukin 15 and activation of the innate immune system by a shorter gluten peptide (p31 43/49).

One protease-resistant peptide from α-gliadin contains a region that stimulates lymphocytes and results in the release of interleukin-15.

For example, sublytic concentrations of PVL, orders of magnitude lower than required for granulocyte lysis, induce release of interleukin-8, leukotriene B4, and reactive oxygen species by PMNs, which contribute to innate host defense against bacteria [26] [28].

This is caused by TLR4-mediated release of interleukin-1B (IL-1B), tumor necrosis factor-alpha (TNFα), and IL-6.