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Identification of a dual JAK3/TEC family kinase inhibitor for atopic dermatitis therapy.
Biochem Pharmacol
January 2025
Center for Drug Safety Evaluation and Research, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058, China; State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China; Taizhou Institute of Zhejiang University, Zhejiang University, Taizhou 318000, China. Electronic address:
Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by recurrent eczematous lesions and severe itching, for which clinical treatments are limited. Selectively inhibiting Janus Kinase 3 (JAK3) and tyrosine kinase expressed in hepatocellular carcinoma (TEC) family kinases is proposed as a promising strategy to treat AD with possible reduced side effects and enhanced efficacy. In this study, we developed a dual JAK3/TEC family kinase inhibitor ZZB, which demonstrated potent inhibitory activity with IC values of 0.
View Article and Find Full Text PDFMultiple Tumors in a Patient with Interleukin-2-Inducible T-Cell Kinase Deficiency: A Case Report.
Int J Mol Sci
December 2024
D.O.P.O. Clinic, Department of Pediatric Hematology and Oncology, IRCCS Giannina Gaslini Institute, 16147 Genoa, Italy.
Immune dysregulation in Inborn Errors of Immunity (IEI) shows a broad phenotype, including autoimmune disorders, benign lymphoproliferation, and malignancies, driven by an increasing number of implicated genes. Recent findings suggest that childhood cancer survivors (CCSs) may exhibit immunological abnormalities potentially linked to an underlying IEI, along with a well-known increased risk of subsequent malignancies due to prior cancer treatments. We describe a patient with two composite heterozygous pathogenic variants in the interleukin-2-inducible T-cell kinase () gene and a history of multiple tumors, including recurrent Epstein-Barr virus (EBV)-related nodular sclerosis and Hodgkin's lymphoma (NSHL), associated with unresponsive multiple hand warts, immune thrombocytopenia, and an impaired immunological profile (CD4+ lymphocytopenia, memory B-cell deficiency, reduction in regulatory T-cells, and B-cell- and T-cell-activated profiles).
View Article and Find Full Text PDFAcalabrutinib in combination with rituximab and lenalidomide in patients with relapsed or refractory follicular lymphoma: Results of the phase 1b open-label study (ACE-LY-003).
Br J Haematol
December 2024
University of North Carolina Lineberger Cancer Center, Chapel Hill, North Carolina, USA.
Patients with relapsed/refractory (R/R) follicular lymphoma (FL) have limited effective treatment options. Bruton tyrosine kinase inhibitors (BTKis) increase the anti-tumoural phenotype of tumour-associated macrophages, providing rationale to combine them with rituximab and lenalidomide (R). Acalabrutinib, a second-generation BTKi, has potential to improve R efficacy without increasing T-cell-mediated toxicity due to its lack of interleukin-2-inducible T-cell kinase inhibition.
View Article and Find Full Text PDFCovalent targeting of splicing in T cells.
Cell Chem Biol
November 2024
Department of Chemical Immunology and Proteomics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. Electronic address:
Article Synopsis
- The study highlights a lack of available chemical probes for proteins involved in splicing, specifically focusing on a compound called EV96 that selectively reduces a protein called ITK in T cells.
- Researchers found that the effectiveness of EV96 varies depending on the T cell state, which is influenced by different protein turnover rates and how ITK mRNA is spliced.
- The paper presents a comprehensive list of proteins tied to splicing and demonstrates that many splicing factors can be targeted using new chemical strategies, showcasing the potential for splicing-targeted therapies in immune response modulation.
Balancing immune activation with Itk.
Trends Pharmacol Sci
November 2024
National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address:
Development of protective immune responses relies on a balance between proinflammatory CD4 T helper (Th) cell populations such as Th17 cells and regulatory CD4 T cells (Tregs) that keep immune activation in check. Evidence that interleukin-2-inducible T cell kinase (Itk) regulates this balance supports therapeutic applications for Itk inhibition.
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