Sentence examples for microbial stimuli and from inspiring English sources

Here we show that GM-CSF i) provokes non-classical monocyte activation; ii) drives monocytes towards an anti-inflammatory phenotype; iii) enhances innate immune functions; iv) primes monocyte responses to secondary microbial stimuli; and v) accelerates epithelial healing via monocytes.

Serum cytokines may therefore represent the response in the intestines as well as the liver to luminal microbial stimuli and may not be identical to intestinal tissue cytokines.

However, osteoblasts also express TLRs and can directly respond to microbial stimuli and secrete inflammatory cytokines such as IL-1 and TNF-α.

HBD3 is another β-defensin family member and is expressed predominantly in the lung, reproductive tract and skin and is induced by microbial stimuli and proinflammatory cytokines 4, 5.

Macrophages mount M1 phenotype in response to microbial stimuli and Interferon gamma (INF- γ): classical activation of macrophages is characterized by high capability to present antigen and high expression of Interleukin 12 (IL-12) and other proinflammatory cytokines, thus being able to trigger T helper 1 (Th1) immune response [ 14, 15].

For example, Tlr2 (Toll-like receptor 2), Tlr4 (toll-like receptor 4), Syk (Spleen tyrosine kinase) and Ebi3 (Epstein-Barr virus induced gene 3) are part of the Toll-like receptor signaling pathway to respond to microbial stimuli (LPS) and induce inflammation (Table 2).

PBMC will be stimulated with various agonists to TLR (bacterial, fungal and viral) and with microbial stimuli.

MAIT cells react to a wide range of microbial stimuli, including Gram-positive and Gram-negative bacteria as well as yeasts [ 61, 62].

Of note, this effect was independent of BCR crosslinking, but dependent on T-cell-derived CD40L and microbial stimuli (activators of Toll-like receptor 9), suggesting that antigen-unspecific bystander activation can influence T-cell polarization [ 25].

Monocytes and neutrophils are known to respond to microbial stimuli by trafficking to infected tissues and secreting inflammatory cytokines.

The response of host immune cells to microbial stimuli is dependent on robust and coordinated gene expression programs involving the transcription of thousands of genes.