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Background: Genetically immunodeficient mice lacking Il2rg and Rag2 genes have been widely utilized in the field of biomedical research. However, immunodeficient rats, which offer the advantage of larger size, have not been as extensively used to date. Recently, Severe Combined Immunodeficiency (SCID) rats were generated using CRISPR/Cas9 system, targeting Il2rg and Rag2 in National BioResource Project in Japan.

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Objective: Genetic associations and blockade of the interleukin-23/IL-17 axis with monoclonal antibodies support a role for this pathway in psoriatic arthritis (PsA). This study examines the requirement of IL-23 for IL-17 production, and the role of the metabolic microenvironment in the expansion of Th-derived cells in PsA.

Methods: PsA patient synovial fluid or peripheral blood Th cell frequencies were evaluated by flow cytometry using CCR6, CD161 and T-bet as phenotypic markers, and the cytokines IFN-γ, GM-CSF and IL-17 assessed by flow cytometry and ELISA.

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Recently, evidence has supported a significant role for immune and oxidative-mediated damage underlying the pathogenesis of different types of retinal diseases, including retinitis pigmentosa (RP). Our study aimed to evaluate the presence of immune cells and mediators in patients with RP using flow cytometric analysis of peripheral blood (PB) and aqueous humor (AH) samples. We recruited 12 patients with RP and nine controls undergoing cataract surgery.

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CCR5 mediates rheumatoid arthritis progression by promoting the activation and proliferation of non-classical Th1 cells.

Int J Rheum Dis

November 2024

Department of Clinical Immunology, Xijing Hospital, and National Translational Science Center for Molecular Medicine, Fourth Military Medical University, Xi'an, Shaanxi, China.

Aim: Rheumatoid arthritis (RA) is a prevalent autoimmune disease characterized by immune dysegulation, including an immune imbalance due to abnormal activation of non-classical Th1 cells (CD161 Th1). This study investigated the effects of CCR5 on the activation and proliferation of CD161 Th1 and their pathogenicity in patients with RA.

Methods: The study was conducted on 53 patients with RA and 32 age- and sex-matched healthy controls (HC).

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Background: High levels of LLT1 expression have been found in several cancers, where it interacts with CD161 on NK cells to facilitate tumor immune escape. Targeting LLT1 could potentially relieve this inhibitory signal and enhance anti-tumor responses mediated through NK cells. Using the 'The Cancer Genome Atlas' (TCGA) database, we investigated the role of LLT1 in the tumor microenvironment (TME) across various cancers.

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