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C-type lectin, which plays an important role in fish innate immunity, was cloned from tilapia and its functional characterization under low-temperature stress is reported. Its ORF is 453 bp, encoding 150 amino acids, and has a 5'UTR of 83 bp, a 3'UTR of 559 bp, and a poly (A) tail. The tilapia C-type lectin genomic DNA was acquired with a length of 5714 bp, containing six exons and five introns. Its promoter sequence was cloned and has a length of 2251 bp. The highest promoter activity occurs in the regulatory region (-900 bp to -450 bp). A hemagglutination assay of recombinant tilapia C-type lectin protein showed positive hemagglutination of rabbit and tilapia erythrocytes. RT-qPCR and western blot assays showed that its expression in the liver, spleen, and intestine were clearly affected by low-temperature stress. Thus, tilapia C-type lectin appear to be affected by abiotic stress, as well as by biological stress.
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http://dx.doi.org/10.1016/j.fsi.2016.10.004 | DOI Listing |
Fish Shellfish Immunol
September 2025
Department of Biology, The Gandhigram Rural Institute (Deemed to be University), Gandhigram, Dindigul, Tamil Nadu 624302, India.
The dynamic interaction between immune recognition molecules and signaling pathways in the innate immune response of Penaeus monodon to White Spot Syndrome Virus (WSSV) infection is unveiled in this study. Through comprehensive gene expression profiling, we demonstrate significant upregulation of key immune genes, including a specific C-type lectin and a defined ficolin isoform, in WSSV-infected hemocytes, underscoring their pivotal roles in pathogen recognition and antiviral defense. Leveraging advanced molecular techniques, we successfully expressed, purified, and characterized these recombinant proteins, revealing their time-dependent expression and high-affinity binding to lipopolysaccharides (LPS).
View Article and Find Full Text PDFTransplant Direct
September 2025
Unidad Transplante de О́rganos, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain.
Extracorporeal photopheresis (ECP) is a well-established, safe, and effective immunomodulatory therapy currently used in clinics to decrease T cell-mediated immunity in various disorders, including autoimmune diseases and chronic rejection in organ transplantation. Although the ECP procedure has been shown to induce apoptotic cells that are reintroduced into the patient at the end of the treatment, the precise tolerogenic mechanisms mediated by ECP are not fully understood. Previous in vitro studies have demonstrated that early apoptotic cells express annexins on their cell surface, which suppress myeloid cell activation on stimulation with bacterial lipopolysaccharide through Toll-like receptors.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
August 2025
Division of Life Sciences and Department of Life Science, Graduate School, CHA University, 13488 Seongnam-si, Gyeonggi-do, Republic of Korea.
Background: Parkinson's disease (PD) is characterized by a progressive decline in dopaminergic neurons within the substantia nigra (SN). Although its underlying cause has yet to be fully elucidated, accumulating evidence suggests that neuroinflammation contributes substantially to disease development. Treatment strategies targeting neuroinflammation could improve PD outcomes.
View Article and Find Full Text PDFOsteoarthritis Cartilage
September 2025
Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Bioengineering, University of Pittsburgh Swanson School of Engineering, Pittsburgh, PA, USA; Orland Bethel Family Musculoskeletal Research Center, University of Pittsburgh School of Med
Objective: Previous studies in our lab demonstrated that estrogen receptor-α (ERα) levels in cartilage decreased with osteoarthritis (OA). We also defined the essential role of ERα in maintaining the health of chondrocytes. However, most of the studies were conducted in vitro, and the physiological link between ERα loss and cartilage degradation has not been demonstrated using animal models.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Biology, Providence College, Providence, Rhode Island, United States of America.
In Npc1 deficient mice, postnatal developmental alterations in cerebellar microglia and Purkinje cells (PCs) are followed by early-onset neurodegeneration. Even in the absence of PC loss, microglia in Npc1nmf164 mice display hallmark features of activation during early postnatal development, including increased proliferation, enhanced phagocytic activity, and morphological changes indicative of an activated state. In this study, we investigated whether mammalian target of rapamycin complex 1 (mTORC1) drives postnatal activation of cerebellar microglia in Npc1nmf164 mice.
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