NLRC5: A Potential Target for Central Nervous System Disorders

Zhang, Lu; Cui, Jiao; Liu, Lingjuan; Wang, Aiping; Tang, Li; Ren, Yi; Huang, Peng; Xu, Jie; Mao, Ding-An

doi:10.3389/fimmu.2021.704989

Cited by 11 publications

(8 citation statements)

References 83 publications

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“…NLRC5 belongs to the family of intracellular PRRs and NOD-like receptors (NLRs) ( 108 ). Immune cells such as monocytes, macrophages, and lymphocytes are known to express NLRC5 at high levels ( 109 ).…”

Section: Nod-like Receptor Family Caspase Recruitment Domain Family D...mentioning

confidence: 99%

Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look

Baig,

Barmpoutsi,

Bharti

et al. 2024

Front. Immunol.

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Macrophages play a central role in initiating, maintaining, and terminating inflammation. For that, macrophages respond to various external stimuli in changing environments through signaling pathways that are tightly regulated and interconnected. This process involves, among others, autoregulatory loops that activate and deactivate macrophages through various cytokines, stimulants, and other chemical mediators. Adaptor proteins play an indispensable role in facilitating various inflammatory signals. These proteins are dynamic and flexible modulators of immune cell signaling and act as molecular bridges between cell surface receptors and intracellular effector molecules. They are involved in regulating physiological inflammation and also contribute significantly to the development of chronic inflammatory processes. This is at least partly due to their involvement in the activation and deactivation of macrophages, leading to changes in the macrophages’ activation/phenotype. This review provides a comprehensive overview of the 20 adaptor molecules and proteins that act as negative regulators of inflammation in macrophages and effectively suppress inflammatory signaling pathways. We emphasize the functional role of adaptors in signal transduction in macrophages and their influence on the phenotypic transition of macrophages from pro-inflammatory M1-like states to anti-inflammatory M2-like phenotypes. This endeavor mainly aims at highlighting and orchestrating the intricate dynamics of adaptor molecules by elucidating the associated key roles along with respective domains and opening avenues for therapeutic and investigative purposes in clinical practice.

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Section: Nod-like Receptor Family Caspase Recruitment Domain Family D...mentioning

confidence: 99%

Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look

Baig,

Barmpoutsi,

Bharti

et al. 2024

Front. Immunol.

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“…Anaphylatoxins are responsible for activating pro-inflammatory signals. C5b, on the other hand, combines with C6, C7, C8, and C9 to form the MAC, which penetrates the cell membrane, leading to cell lysis upon target surfaces, playing a role in the innate immune process and mediating the killing and clearance of pathogens [9] (Fig. 1).…”

Section: Complement Pathwaysmentioning

confidence: 99%

The complement system: a potential target for the comorbidity of chronic pain and depression

Tang,

Hu,

Zou

et al. 2024

Korean J Pain

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The mechanisms of the chronic pain and depression comorbidity have gained significant attention in recent years. The complement system, widely involved in central nervous system diseases and mediating non-specific immune mechanisms in the body, remains incompletely understood in its involvement in the comorbidity mechanisms of chronic pain and depression. This review aims to consolidate the findings from recent studies on the complement system in chronic pain and depression, proposing that it may serve as a promising shared therapeutic target for both conditions. Complement proteins C1q, C3, C5, as well as their cleavage products C3a and C5a, along with the associated receptors C3aR, CR3, and C5aR, are believed to have significant implications in the comorbid mechanism. The primary potential mechanisms encompass the involvement of the complement cascade C1q/C3-CR3 in the activation of microglia and synaptic pruning in the amygdala and hippocampus, the role of complement cascade C3/C3a-C3aR in the interaction between astrocytes and microglia, leading to synaptic pruning, and the C3a-C3aR axis and C5a-C5aR axis to trigger inflammation within the central nervous system. We focus on studies on the role of the complement system in the comorbid mechanisms of chronic pain and depression.

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“…Different DNA methylations of NLRP2 between females and males affected SARS-CoV-2 infection and the outcome of COVID-19 disease [ 95 ]. Astrocytes have been shown to express NLRP2, NLRP3, and NLRC4 and NLRC5 [ 89 , 96 , 97 , 98 ]. Reactive astrocytes upregulate NLRP3 and NLRC4 [ 97 ], yet signaling patterns of inflammasome priming and activation in virus infected in astrocytes remain to be revealed.…”

Section: Immune Responses Of Virus-infected Astrocytesmentioning

confidence: 99%

Immune Functions of Astrocytes in Viral Neuroinfections

Jorgačevski

Potokar

2023

IJMS

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Neuroinfections of the central nervous system (CNS) can be triggered by various pathogens. Viruses are the most widespread and have the potential to induce long-term neurologic symptoms with potentially lethal outcomes. In addition to directly affecting their host cells and inducing immediate changes in a plethora of cellular processes, viral infections of the CNS also trigger an intense immune response. Regulation of the innate immune response in the CNS depends not only on microglia, which are fundamental immune cells of the CNS, but also on astrocytes. These cells align blood vessels and ventricle cavities, and consequently, they are one of the first cell types to become infected after the virus breaches the CNS. Moreover, astrocytes are increasingly recognized as a potential viral reservoir in the CNS; therefore, the immune response initiated by the presence of intracellular virus particles may have a profound effect on cellular and tissue physiology and morphology. These changes should be addressed in terms of persisting infections because they may contribute to recurring neurologic sequelae. To date, infections of astrocytes with different viruses originating from genetically distinct families, including Flaviviridae, Coronaviridae, Retroviridae, Togaviridae, Paramyxoviridae, Picomaviridae, Rhabdoviridae, and Herpesviridae, have been confirmed. Astrocytes express a plethora of receptors that detect viral particles and trigger signaling cascades, leading to an innate immune response. In this review, we summarize the current knowledge on virus receptors that initiate the release of inflammatory cytokines from astrocytes and depict the involvement of astrocytes in immune functions of the CNS.

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NLRC5: A Potential Target for Central Nervous System Disorders

Cited by 11 publications

References 83 publications

Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look

Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look

The complement system: a potential target for the comorbidity of chronic pain and depression

Immune Functions of Astrocytes in Viral Neuroinfections

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