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The adaptor protein CARD9, from fungal immunity to tumorigenesis.

ABSTRACT: The adaptor protein CARD9 is in charge of mediating signals from PRRs of myeloid cells to downstream transcription factor NF-?B. CARD9 plays an indispensable role in innate immunity. Both mice and humans with CARD9 deficiency show increased susceptibility to fungal and bacterial infections. CARD9 signaling not only activates but also shapes adaptive immune responses. The role of this molecule in tumor progression is increasingly being revealed. Our early study found that CARD9 is associated with the development of colon cancer and functions as a regulator of antitumor immunity. In this review, we focus on the upstream and downstream signaling pathways of CARD9, then we summarize the immunological recognition and responses induced by CARD9 signaling. Furthermore, we review the function of CARD9 in multiple aspects of host immunity, ranging from fungal immunity to tumorigenesis.

SUBMITTER: Wang Y

PROVIDER: S-EPMC7471374 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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The adaptor protein CARD9, from fungal immunity to tumorigenesis.

Wang Ying Y Zhang Di D Hou Yayi Y Shen Sunan S Wang Tingting T

American journal of cancer research 20200801 8

The adaptor protein CARD9 is in charge of mediating signals from PRRs of myeloid cells to downstream transcription factor NF-κB. CARD9 plays an indispensable role in innate immunity. Both mice and humans with CARD9 deficiency show increased susceptibility to fungal and bacterial infections. CARD9 signaling not only activates but also shapes adaptive immune responses. The role of this molecule in tumor progression is increasingly being revealed. Our early study found that CARD9 is associated with ...[more]

PMID: 32905547

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Project description:UnlabelledDengue virus (DENV) is the most common mosquito-borne virus infecting humans and is currently a serious global health challenge. To establish infection in its host cells, DENV must subvert the production and/or antiviral effects of interferon (IFN). The aim of this study was to understand the mechanisms by which DENV suppresses IFN production. We determined that DENV NS4A interacts with mitochondrial antiviral signaling protein (MAVS), which was previously found to activate NF-κB and IFN regulatory factor 3 (IRF3), thus inducing type I IFN in the mitochondrion-associated endoplasmic reticulum membranes (MAMs). We further demonstrated that NS4A is associated with the N-terminal CARD-like (CL) domain and the C-terminal transmembrane (TM) domain of MAVS. This association prevented the binding of MAVS to RIG-I, resulting in the repression of RIG-I-induced IRF3 activation and, consequently, the abrogation of IFN production. Collectively, our findings illustrate a new molecular mechanism by which DENV evades the host immune system and suggest new targets for anti-DENV strategies.ImportanceType I interferon (IFN) constitutes the first line of host defense against invading viruses. To successfully establish infection, dengue virus (DENV) must counteract either the production or the function of IFN. The mechanism by which DENV suppresses IFN production is poorly understood and characterized. In this study, we demonstrate that the DENV NS4A protein plays an important role in suppressing interferon production through binding MAVS and disrupting the RIG-I-MAVS interaction in mitochondrion-associated endoplasmic reticulum membranes (MAMs). Our study reveals that MAVS is a novel host target of NS4A and provides a molecular mechanism for DENV evasion of the host innate immune response. These findings have important implications for understanding the pathogenesis of DENV and may provide new insights into using NS4A as a therapeutic and/or prevention target.

Dataset Information

The adaptor protein CARD9, from fungal immunity to tumorigenesis.

Publications

The adaptor protein CARD9, from fungal immunity to tumorigenesis.

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