Abstract
Innate immunity activates the corresponding immune response relying on multiple pattern recognition receptors (PRRs) that includes pattern recognition receptors (PRRs), like NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), and C-type lectin receptors (CLRs), which could accurately recognize invasive pathogens. In particular, NLRs belong to a large protein family of pattern recognition receptors in the cytoplasm, where they are highly correlated with activation of inflammatory response system followed by rapid clearance of invasive pathogens. Among the NLRs family, NLRC5, also known as NOD4 or NOD27, accounts for a large proportion and involves in immune responses far and wide. Notably, in the above response case of inflammation, the expression of NLRC5 remarkably increased in immune cells and immune-related tissues. However, the evidence for higher expression of NLRC5 in immune disease still remains controversial. It is noted that the growing evidence further accounts for the participation of NLRC5 in the innate immune response and inflammatory diseases. Moreover, NLRC5 has also been confirmed to exert a critical role in the control of regulatory diverse signaling pathways. Together with its broad participation in the occurrence and development of immune diseases, NLRC5 can be consequently treated as a potential therapeutic target. Nevertheless, the paucity of absolute understanding of intrinsic characteristics and underlying mechanisms of NLRC5 still make it hard to develop targeting drugs. Therefore, current summary about NLRC5 information is indispensable. Herein, current knowledge of NLRC5 is summarized, and research advances in terms of NLRC5 in characteristics, biological function, and regulatory mechanisms are reviewed.
Highlights
The innate immune system has always been a striker against pathogenic microorganisms such as bacteria, fungi, and viruses (Akira et al, 2006; Medzhitov, 2007)
NLRC5 may take an active part in the occurrence and reversal of hepatic fibrosis. These findings provide essential proof of the principle that NLRC5 may represent a target for the prevention or treatment of liver fibrosis
Recent advance have found that silencing NLRC5 could significantly inhibit proliferation, extracellular matrix (ECM) deposition, and pro-fibrotic molecules expression in CFs (Yang et al, 2019). These results initially suggested that NLRC5 has a regulatory effect on accelerating myocardial fibrosis, which involves in heart disease
Summary
The innate immune system has always been a striker against pathogenic microorganisms such as bacteria, fungi, and viruses (Akira et al, 2006; Medzhitov, 2007). Innate immunity is responsible for most inflammatory responses, and the stress of innate immunity reflects the status of the pathogen-specific adaptive immunity (Janeway and Medzhitov, 2002; Beutler, 2004). Innate immunity activates the corresponding immune response, requiring multiple pattern recognition receptors (PRRs) that recognize the molecular structures of specific pathogens in different cellular components, such as the cytoplasmic membrane, endosomes, and cytoplasm (Janeway, 1989; Kumar et al, 2009). Despite relatively large differences in their structures, expressions, and localizations, all of them can recognize invading pathogens and further initiate the innate and adaptive immune response when organism suffers from intrusion of non-self ’s pathogens (Table 1) (Yoneyama and Fujita, 2009; Dixit and Kagan, 2013; Dambuza and Brown, 2015; Kouli et al, 2019). This paper aims to provide a comprehensive update on the diverse pharmacological roles of NLRC5 in the process of immune diseases, especially on liver diseases, renal diseases, rheumatoid arthritis, heart diseases, lung diseases, and spleen diseases
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