English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

In a recent paper, Dring et al. (1) showed that natural killer (NK) cell-associated killer cell Ig-like receptors (KIR) gene KIR2DS3 and IL28B (IFNλ3) T allele are associated with chronic hepatitis C, confirming earlier reports (2, 3). Interestingly, they showed that the presence of both genetic markers synergistically increased the risk of chronic infection over either factor alone (1). As a potential explanation for this finding, they presented experimental data suggesting that IL28A inhibits IFN-γ secretion by NK cells (1). Thus, Dring et al. (1) proposed a functional link between NK cells and λ-IFNs. This finding is unexpected because IFN-λR1, the natural receptor of λ-IFNs, has been shown to display a rather restricted expression pattern, limiting the response to λ-IFNs to primarily epithelium-like tissues, whereas leukocytes do not respond to IFN-λ (2). In line with the previously reported absence of IFN-λR1 on hemopoietic cells (4), we could not detect IFN-λR1 surface expression on freshly isolated NK cells from healthy donors …

Do λ-IFNs IL28A and IL28B act on human natural killer cells?