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Important Role of the IL-32 Inflammatory Network in the Host Response against Viral Infection.

Zhou Y, Zhu Y - Viruses (2015)

Bottom Line: Since the discovery of IL-32 in 2005, our appreciation for its diverse roles continues to grow.Recent studies have discovered the antiviral effects induced by IL-32 and its associated regulatory mechanisms.The interactions between IL-32 and various cytokines including cyclooxygenase 2 (COX-2), inducible nitric oxide synthase (iNOS), interferon (IFN)-λ1, interleukin (IL)-6, and soluble IL-6 receptor have been described.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China. zhouyq1993@whu.edu.cn.

ABSTRACT
The pro-inflammatory cytokine interleukin (IL)-32 has gained much attention recently because of its important role in the inflammatory network. Since the discovery of IL-32 in 2005, our appreciation for its diverse roles continues to grow. Recent studies have discovered the antiviral effects induced by IL-32 and its associated regulatory mechanisms. The interactions between IL-32 and various cytokines including cyclooxygenase 2 (COX-2), inducible nitric oxide synthase (iNOS), interferon (IFN)-λ1, interleukin (IL)-6, and soluble IL-6 receptor have been described. This review aims to integrate these new findings into explicit concepts and raises the intriguing possibility of IL-32 as a therapeutic target.

No MeSH data available.


Related in: MedlinePlus

The IL-32-mediated inflammatory network against viral infection. Virus infection induces COX-2 and sIL-6R expression, which upregulates IL-32 production, resulting in increases of iNOS, IFN-λ1, and IL-6 levels. However, elevated IL-32 level feedback inhibits COX-2 and sIL-6R expression; iNOS also has a negative feedback effect on IL-32. This network plays a key role in host response to viral infection.
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viruses-07-02762-f001: The IL-32-mediated inflammatory network against viral infection. Virus infection induces COX-2 and sIL-6R expression, which upregulates IL-32 production, resulting in increases of iNOS, IFN-λ1, and IL-6 levels. However, elevated IL-32 level feedback inhibits COX-2 and sIL-6R expression; iNOS also has a negative feedback effect on IL-32. This network plays a key role in host response to viral infection.

Mentions: Together, a schematic diagram for the antiviral action of IL-32 is presented in Figure 1.


Important Role of the IL-32 Inflammatory Network in the Host Response against Viral Infection.

Zhou Y, Zhu Y - Viruses (2015)

The IL-32-mediated inflammatory network against viral infection. Virus infection induces COX-2 and sIL-6R expression, which upregulates IL-32 production, resulting in increases of iNOS, IFN-λ1, and IL-6 levels. However, elevated IL-32 level feedback inhibits COX-2 and sIL-6R expression; iNOS also has a negative feedback effect on IL-32. This network plays a key role in host response to viral infection.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4488729&req=5

viruses-07-02762-f001: The IL-32-mediated inflammatory network against viral infection. Virus infection induces COX-2 and sIL-6R expression, which upregulates IL-32 production, resulting in increases of iNOS, IFN-λ1, and IL-6 levels. However, elevated IL-32 level feedback inhibits COX-2 and sIL-6R expression; iNOS also has a negative feedback effect on IL-32. This network plays a key role in host response to viral infection.
Mentions: Together, a schematic diagram for the antiviral action of IL-32 is presented in Figure 1.

Bottom Line: Since the discovery of IL-32 in 2005, our appreciation for its diverse roles continues to grow.Recent studies have discovered the antiviral effects induced by IL-32 and its associated regulatory mechanisms.The interactions between IL-32 and various cytokines including cyclooxygenase 2 (COX-2), inducible nitric oxide synthase (iNOS), interferon (IFN)-λ1, interleukin (IL)-6, and soluble IL-6 receptor have been described.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China. zhouyq1993@whu.edu.cn.

ABSTRACT
The pro-inflammatory cytokine interleukin (IL)-32 has gained much attention recently because of its important role in the inflammatory network. Since the discovery of IL-32 in 2005, our appreciation for its diverse roles continues to grow. Recent studies have discovered the antiviral effects induced by IL-32 and its associated regulatory mechanisms. The interactions between IL-32 and various cytokines including cyclooxygenase 2 (COX-2), inducible nitric oxide synthase (iNOS), interferon (IFN)-λ1, interleukin (IL)-6, and soluble IL-6 receptor have been described. This review aims to integrate these new findings into explicit concepts and raises the intriguing possibility of IL-32 as a therapeutic target.

No MeSH data available.


Related in: MedlinePlus