Research ArticleInflammation

The early synthesis of p35 and activation of CDK5 in LPS-stimulated macrophages suppresses interleukin-10 production

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Science Signaling  24 Nov 2015:
Vol. 8, Issue 404, pp. ra121
DOI: 10.1126/scisignal.aab3156

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  • RE: Fine tuning of IL-10 signalling by microRNAs in TB

    The anti-inflammatory cytokine IL10 belongs to the clsss-2 cytokine family [includes IL19, 20, 22, 24, 26, interferon (IFN alpha, beta, epsilon, kappa, omega, tau, delta, gamma) and interferon-like molecules (limitin, IL28A, IL28B and IL29)] and functions as master regulator of immunity and infection. During bacterial, viral and protozoal infection, the communication between PAMPs and PRRs of APCs directs the development of Th1, Th2 and Treg cell populations, depending on cytokines, chemokine environment and state of co-stimulation. The regulatory response conditions involving IL10 can act in an autocrine manner to suppress the activity of NK cells, macrophages and Th1 cells, all of which are obligatory for pathogen clearance can add to tissue injury. So, IL10 mediates both pathogen clearance and protection of host from inflammatory shock. Bacterial LPS (a PAMP) activates TLR signalling that in turn directs production of both inflammatory and anti-inflammatory responses in a time-dependent manner, but how this tightly regulated mechanism is managed for IL10 is least understood.

    Na et al. found that LPS stimulation of macrophages not only produces inflammatory cytokines, but also transiently stimulates synthesis of p35 that binds to and stimulates CDK5. The mapping of protein-protein interaction clearly demonstrates that the CDK5-p35 (CDK5R1) complex binds to the IL10 promoter, preventing innate immune cells from producing IL10. Furthermore the LPS-stimulat...

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