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A20‐binding inhibitor of NF‐κB activation (ABIN1) is a polyubiquitin‐binding protein that regulates cell death and immune responses. Although Abin1 is located on chromosome 5q in the region commonly deleted in patients with 5q minus syndrome, the most distinct of the myelodysplastic syndromes (MDSs), the precise role of ABIN1 in MDSs remains unknown. In this study, mice with a mutation disrupting the polyubiquitin‐binding site (Abin1Q478H/Q478H) is generated. These mice develop MDS‐like diseases characterized by anemia, thrombocytopenia, and megakaryocyte dysplasia. Extramedullary hematopoiesis and bone marrow failure are also observed in Abin1Q478H/Q478H mice. Although Abin1Q478H/Q478H cells are sensitive to RIPK1 kinase–RIPK3–MLKL‐dependent necroptosis, only anemia and splenomegaly are alleviated by RIPK3 deficiency but not by MLKL deficiency or the RIPK1 kinase‐dead mutation. This indicates that the necroptosis‐independent function of RIPK3 is critical for anemia development in Abin1Q478H/Q478H mice. Notably, Abin1Q478H/Q478H mice exhibit higher levels of type I interferon (IFN‐I) expression in bone marrow cells compared towild‐type mice. Consistently, blocking type I IFN signaling through the co‐deletion of Ifnar1 greatly ameliorated anemia, thrombocytopenia, and splenomegaly in Abin1Q478H/Q478H mice. Together, these results demonstrates that ABIN1(Q478) prevents the development of hematopoietic deficiencies by regulating type I IFN expression. [ABSTRACT FROM AUTHOR]

The replication of HBV in hepatocytes can be effectively inhibited by lifelong antiviral therapy. Because of the long‐term presence of HBV reservoirs, the virus rebound frequently occurs once the treatment is stopped, which poses a considerable obstacle to the complete removal of the virus. In terms of gene composition, regulation of B cell action and function, CXCR5+CD8+ T cells are similar to CXCR5+CD4+ T follicular helper cells, while these cells are characterized by elevated programmed cell death 1 and cytotoxic‐related proteins. CXCR5+CD8+T cells are strongly associated with progression in inflammatory and autoimmune diseases. In addition, CXCR5 expression on the surface of CD8+ T cells is mostly an indicator of memory stem cell‐like failure in progenitor cells in cancer that are more responsive to immune checkpoint blocking therapy. Furthermore, the phenomena have also been demonstrated in some viral infections, highlighting the duality of the cellular immune response of CXCR5+CD8+ T cells. This mini‐review will focus on the function of CXCR5+CD8+ T cells in HBV infection and discuss the function of these CD8+ T cells and the potential of associated co‐stimulators or cytokines in HBV therapeutic strategies. [ABSTRACT FROM AUTHOR]

Most multiplex nucleic acids detection methods require numerous reagents and high‐priced instruments. The emerging clustered regularly interspaced short palindromic repeats (CRISPR)/Cas has been regarded as a promising point‐of‐care (POC) strategy for nucleic acids detection. However, how to achieve CRISPR/Cas multiplex biosensing remains a challenge. Here, an affordable means termed CRISPR‐RDB (CRISPR‐based reverse dot blot) for multiplex target detection in parallel, which possesses the advantages of high sensitivity and specificity, cost‐effectiveness, instrument‐free, ease to use, and visualization is reported. CRISPR‐RDB integrates the trans‐cleavage activity of CRISPR‐Cas12a with a commercial RDB technique. It utilizes different Cas12a‐crRNA complexes to separately identify multiple targets in one sample and converts targeted information into colorimetric signals on a piece of accessible nylon membrane that attaches corresponding specific‐oligonucleotide probes. It has demonstrated that the versatility of CRISPR‐RDB by constructing a four‐channel system to simultaneously detect influenza A, influenza B, respiratory syncytial virus, and SARS‐CoV‐2. With a simple modification of crRNAs, the CRISPR‐RDB can be modified to detect human papillomavirus, saving two‐thirds of the time compared to a commercial PCR‐RDB kit. Further, a user‐friendly microchip system for convenient use, as well as a smartphone app for signal interpretation, is engineered. CRISPR‐RDB represents a desirable option for multiplexed biosensing and on‐site diagnosis. [ABSTRACT FROM AUTHOR]

Innate lymphoid cells (ILCs) are the main resident lymphocytes that mostly reside in tissues owing to the lack of adaptive antigen receptors. These cells are involved in early anti-infective immunity, antitumour immunity, regulation of tissue inflammation, and maintenance of homeostasis in the internal environment of tissues and have been referred to as the “first armies stationed in the human body”. ILCs are widely distributed in the lungs, colon, lymph nodes, oral mucosa and even embryonic tissues. Due to the advantage of their distribution location, they are often among the first cells to come into contact with pathogens.Relevant studies have demonstrated that ILCs play an early role in the defence against a variety of pathogenic microorganisms, including bacteria, viruses, fungi and helminths, before they intervene in the adaptive immune system. ILCs can initiate a rapid, nonspecific response against pathogens prior to the initiation of an adaptive immune response and can generate a protective immune response against specific pathogens, secreting different effectors to play a role.There is growing evidence that ILCs play an important role in host control of infectious diseases. In this paper, we summarize and discuss the current known infectious diseases in which ILCs are involved and ILC contribution to the defence against infectious diseases. Further insights into the mechanisms of ILCs action in different infectious diseases will be useful in facilitating the development of therapeutic strategies for early control of infections. [ABSTRACT FROM AUTHOR]