Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1073/pnas.2501381122 http://scihub22266oqcxt.onion/10.1073/pnas.2501381122 41359845!?!41359845 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41359845&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Proc+Natl+Acad+Sci+U+S+A 2025 ; 122 (50): e2501381122 Nephropedia Template TP {{tp|p=41359845|t=2025. Galectin-9 binding to HLA-DR in dendritic cells controls immune synapse formation and T cell proliferation |pdf=|usr=}}{{41359845}} gab.com Text Galectin-9 binding to HLA-DR in dendritic cells controls immune synapse formation and T cell proliferation JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=41359845 #FOAvip To initiate T cell-mediated immunity, dendritic cells (DCs) present antigens to T cells through the establishment of an immune synapse (IS). While events behind IS formation in T cells are well understood, the organization of IS components at the DC membrane remains ill-defined. Galectins modulate immune responses via glycan-(in)dependent interactions but the molecular mechanisms underlying their function in DC-mediated T cell activation, are poorly described. Here, we demonstrate that intracellular galectin-9 (gal9) in DCs is required for CD4(+) T cell activation through its interaction with the HLA-DR alpha- and beta- cytoplasmic domains, as supported by coimmunoprecipitation, mass spectrometry, and NMR analyses. Live-cell imaging revealed gal9-depleted DCs fail to establish stable ISs with T cells, reducing T cell activation and proliferation. Notably, HLA-DR membrane lateral mobility and recruitment to the IS was diminished in DCs lacking gal9. Conditional gal9 knockout in DCs led to enhanced tumor growth in vivo, underscoring a role for gal9 in T cell-dependent antitumor immunity. Collectively, this study reports gal9-mediated HLA-DR organization at the DC synapse, uncovering a mechanism through which intracellular galectins coordinate immune receptor positioning to enhance CD4(+) T cell activation. Twit Text FOAVip Galectin-9 binding to HLA-DR in dendritic cells controls immune synapse formation and T cell proliferation ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=41359845 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41359845 #FOAvip English Wikipedia <ref>{{Cite pmid|41359845}}</ref> Galectin-9 binding to HLA-DR in dendritic cells controls immune synapse formation and T cell proliferation #MMPMID41359845 Rodgers-Furones A; Brands T; van Gameren G; Florencio-Zabaleta M; Bathini M; Delgado S; Wijfjes Z; Fedorova K; Classens R; Kroese L; Verdoes M; van Mierlo G; Jimenez-Barbero J; Lindeboom RGH; Arda A; van Spriel AB; Cano LQ Proc Natl Acad Sci U S A 2025[Dec]; 122 (50): e2501381122 PMID41359845show ga To initiate T cell-mediated immunity, dendritic cells (DCs) present antigens to T cells through the establishment of an immune synapse (IS). While events behind IS formation in T cells are well understood, the organization of IS components at the DC membrane remains ill-defined. Galectins modulate immune responses via glycan-(in)dependent interactions but the molecular mechanisms underlying their function in DC-mediated T cell activation, are poorly described. Here, we demonstrate that intracellular galectin-9 (gal9) in DCs is required for CD4(+) T cell activation through its interaction with the HLA-DR alpha- and beta- cytoplasmic domains, as supported by coimmunoprecipitation, mass spectrometry, and NMR analyses. Live-cell imaging revealed gal9-depleted DCs fail to establish stable ISs with T cells, reducing T cell activation and proliferation. Notably, HLA-DR membrane lateral mobility and recruitment to the IS was diminished in DCs lacking gal9. Conditional gal9 knockout in DCs led to enhanced tumor growth in vivo, underscoring a role for gal9 in T cell-dependent antitumor immunity. Collectively, this study reports gal9-mediated HLA-DR organization at the DC synapse, uncovering a mechanism through which intracellular galectins coordinate immune receptor positioning to enhance CD4(+) T cell activation. |*CD4-Positive T-Lymphocytes/immunology[MESH] |*Dendritic Cells/immunology/metabolism[MESH] |*Galectins/metabolism/genetics/immunology[MESH] |*HLA-DR Antigens/metabolism/immunology[MESH] |*Immunological Synapses/immunology/metabolism[MESH] |*T-Lymphocytes/immunology[MESH] |Animals[MESH] |Cell Proliferation[MESH] |Humans[MESH] |Lymphocyte Activation/immunology[MESH] |Mice[MESH]Galectin-9 binding to HLA-DR in dendritic cells controls immune synaps(epmc).pdf DeepDyve Pubget Overpricing