Mucosal immunity and tRNA, tRF, and tiRNA
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REVIEW
Mucosal immunity and tRNA, tRF, and tiRNA Yueying Chen 1,2,3 & Jun Shen 1,2,3 Received: 16 September 2020 / Revised: 15 October 2020 / Accepted: 6 November 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Mucosal immunity has crucial roles in human diseases such as respiratory tract infection, inflammatory bowel diseases (IBD), and colorectal cancer (CRC). Recent studies suggest that the mononuclear phagocyte system, cancer cells, bacteria, and viruses induce the mucosal immune reaction by various pathways, and can be major factors in the pathogenesis of these diseases. Transfer RNA (tRNA) and its fragments, including tRNA-derived RNA fragments (tRFs) and tRNA-derived stress-induced RNAs (tiRNAs), have emerged as a hot topic in recent years. They not only are verified as essential for transcription and translation but also play roles in cellular homeostasis and functions, such as cell metastasis, proliferation, and apoptosis. However, the specific relationship between their biological regulation and mucosal immunity remains unclear to date. In the present review, we carry out a comprehensive discussion on the specific roles of tRNA, tRFs, and tiRNAs relevant to mucosal immunity and related diseases. Keywords Mucosal immunity . Transfer RNA (tRNA) . tRNA-derived RNA fragments (tRFs) . tRNA-derived stress-induced RNAs (tiRNAs)
Introduction The mucosal immune system comprises mucosa-associated lymphoid tissues (MALTs), which exist in the gastrointestinal tract, respiratory organs, the mammary glands, and other parts of the human body. Mucosal immune overreaction and destruction can cause illness. Inflammatory bowel disease (IBD) has been linked to dysfunctional mucosal immunity, and the mucosal immunity analysis showed that regulatory T cells, Th17 cells, and cytokines related to mucosal immunity played a role in IBD [1–4]. It has been revealed that compromised mucosal immune contributed to the progressive systemic inflammation and fibrosis of chronic kidney disease [5, 6].
* Jun Shen [email protected] 1
Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Inflammatory Bowel Disease Research Center, 160# Pu Jian Ave, Shanghai 200127, China
2
Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 160# Pu Jian Ave, Shanghai 200127, China
3
Shanghai Institute of Digestive Disease, 160# Pu Jian Ave, Shanghai 200127, China
A study found that induced mucosal immunity could impede the progression of pertussis [7]. Research also suggested the dysfunction of mucosal immunity resulted in gastrointestinal allergic inflammation [8]. Mucosal immune response can be induced by factors such as bacteria, virus, and tumor cells. When bacteria and viruses invade, the mucosal immune system can be instantly activated to remove the pathogens [9]. However, immune overreaction can induce immunopathological damage [10]. Transfer RNA (tRNA) is a ubiquitous nucleic acid produced by PolIII enzyme, which synthesizes precursor
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