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| http://dx.doi.org/10.1182/blood-2015-07-657999 | DOI Listing |
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Cervical lymph nodes and ovarian teratomas as germinal centres in NMDA receptor-antibody encephalitis.
Brain
August 2022
Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
Autoantibodies against the extracellular domain of the N-methyl-d-aspartate receptor (NMDAR) NR1 subunit cause a severe and common form of encephalitis. To better understand their generation, we aimed to characterize and identify human germinal centres actively participating in NMDAR-specific autoimmunization by sampling patient blood, CSF, ovarian teratoma tissue and, directly from the putative site of human CNS lymphatic drainage, cervical lymph nodes. From serum, both NR1-IgA and NR1-IgM were detected more frequently in NMDAR-antibody encephalitis patients versus controls (both P < 0.
View Article and Find Full Text PDFScreening and development of monoclonal antibodies for identification of ferret T follicular helper cells.
Sci Rep
January 2021
Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, VIC, Australia.
The ferret is a key animal model for investigating the pathogenicity and transmissibility of important human viruses, and for the pre-clinical assessment of vaccines. However, relatively little is known about the ferret immune system, due in part to a paucity of ferret-reactive reagents. In particular, T follicular helper (Tfh) cells are critical in the generation of effective humoral responses in humans, mice and other animal models but to date it has not been possible to identify Tfh in ferrets.
View Article and Find Full Text PDFUnique Immune Cell Coactivators Specify Locus Control Region Function and Cell Stage.
Mol Cell
December 2020
Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY 10065, USA. Electronic address:
Locus control region (LCR) functions define cellular identity and have critical roles in diseases such as cancer, although the hierarchy of structural components and associated factors that drive functionality are incompletely understood. Here we show that OCA-B, a B cell-specific coactivator essential for germinal center (GC) formation, forms a ternary complex with the lymphoid-enriched OCT2 and GC-specific MEF2B transcription factors and that this complex occupies and activates an LCR that regulates the BCL6 proto-oncogene and is uniquely required by normal and malignant GC B cells. Mechanistically, through OCA-B-MED1 interactions, this complex is required for Mediator association with the BCL6 promoter.
View Article and Find Full Text PDFSignalling input from divergent pathways subverts B cell transformation.
Nature
July 2020
Department of Systems Biology, City of Hope Comprehensive Cancer Center, Monrovia, CA, USA.
Article Synopsis
- * Common mutations, such as those activating STAT5 and ERK proteins, typically do not occur together, which indicates competition between pathways that lead to cancer development, with each pathway engaging different biochemical responses mediated by transcription factors MYC and BCL6.
- * Reactivating the suppressed divergent pathways can counteract the main oncogenic driver, suggesting that targeting these pathways could improve treatment strategies for leukaemia.
GITR Agonism Triggers Antitumor Immune Responses through IL21-Expressing Follicular Helper T Cells.
Cancer Immunol Res
May 2020
Laboratory of Immunology, Research Institute of Pharmaceutical Science, College of Pharmacy, Seoul National University, Seoul, Republic of Korea.
Although treatment with the glucocorticoid-induced tumor necrosis factor receptor-related protein (GITR) agonistic antibody (DTA-1) has shown antitumor activity in various tumor models, the underlying mechanism is not fully understood. Here, we demonstrate that interleukin (IL)-21-producing follicular helper T (Tfh) cells play a crucial role in DTA-1-induced tumor inhibition. The administration of DTA-1 increased IL21 expression by Tfh cells in an antigen-specific manner, and this activation led to enhanced antitumor cytotoxic T lymphocyte (CTL) activity.
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