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10.4049/jimmunol.1201363 http://scihub22266oqcxt.onion/10.4049/jimmunol.1201363 C3680117!3680117 !23686488     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23686488 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cross talk between follicular Th cells and tumor cells in human follicular lymphoma promotes immune evasion in the tumor microenvironment |pdf=|usr=}}{{23686488 }} gab.com Text Cross talk between follicular Th cells and tumor cells in human follicular lymphoma promotes immune evasion in the tumor microenvironment JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23686488 #FOAvip The microenvironment of human follicular lymphoma (FL), an incurable B cell non-Hodgkin's lymphoma, is thought to play a major role in its pathogenesis and course. Microenvironmental cells of likely importance include follicular Th cells (TFH) and regulatory T cells (Tregs), and understanding their interactions with FL tumor cells is necessary to develop novel therapeutic strategies. We found that IL-4 and CD40L are expressed by intratumoral TFH and induce production of CCL17 and CCL22 by FL tumor cells. IL-4 alone induces only CCL17 but enhances stimulation by CD40L of both CCL17 and CCL22. Consistent with our in vitro results, mRNA transcripts of IL-4 correlated with CCL17, but not CCL22, in gene expression profiling studies of FL biopsies, whereas CD40L correlated with both CCL17 and CCL22. Tumor supernatants induced preferential migration of Tregs and IL-4-producing T cells rather than IFN-?-producing T cells, and Abs to CCR4 significantly abrogated the migration of Tregs. Our results suggest that through two distinct mechanisms, intratumoral TFH induce production of CCL17 and CCL22 by FL tumor cells and facilitate active recruitment of Tregs and IL-4-producing T cells, which, in turn, may stimulate more chemokine production in a feed-forward cycle. Thus, TFH appear to play a major role in generating an immunosuppressive tumor microenvironment that promotes immune escape and tumor survival and growth. Our results provide novel insights into the cross talk among TFH, tumor cells, and Tregs in FL, and offer potential targets for development of therapeutic strategies to overcome immune evasion. Twit Text FOAVip Cross talk between follicular Th cells and tumor cells in human follicular lymphoma promotes immune evasion in the tumor microenvironment ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23686488 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23686488 #FOAvip English Wikipedia <ref>{{Cite pmid|23686488 }}</ref> Cross talk between follicular Th cells and tumor cells in human follicular lymphoma promotes immune evasion in the tumor microenvironment #MMPMID23686488 Rawal S ; Chu F ; Zhang M ; Park HJ ; Nattamai D ; Kannan S ; Sharma R ; Delgado D ; Chou T ; Lin HY ; Baladandayuthapani V ; Luong A ; Vega F ; Fowler N ; Dong C ; Davis RE ; Neelapu SS J Immunol 2013[Jun]; 190 (12 ): 6681-93 PMID23686488 show ga The microenvironment of human follicular lymphoma (FL), an incurable B cell non-Hodgkin's lymphoma, is thought to play a major role in its pathogenesis and course. Microenvironmental cells of likely importance include follicular Th cells (TFH) and regulatory T cells (Tregs), and understanding their interactions with FL tumor cells is necessary to develop novel therapeutic strategies. We found that IL-4 and CD40L are expressed by intratumoral TFH and induce production of CCL17 and CCL22 by FL tumor cells. IL-4 alone induces only CCL17 but enhances stimulation by CD40L of both CCL17 and CCL22. Consistent with our in vitro results, mRNA transcripts of IL-4 correlated with CCL17, but not CCL22, in gene expression profiling studies of FL biopsies, whereas CD40L correlated with both CCL17 and CCL22. Tumor supernatants induced preferential migration of Tregs and IL-4-producing T cells rather than IFN-?-producing T cells, and Abs to CCR4 significantly abrogated the migration of Tregs. Our results suggest that through two distinct mechanisms, intratumoral TFH induce production of CCL17 and CCL22 by FL tumor cells and facilitate active recruitment of Tregs and IL-4-producing T cells, which, in turn, may stimulate more chemokine production in a feed-forward cycle. Thus, TFH appear to play a major role in generating an immunosuppressive tumor microenvironment that promotes immune escape and tumor survival and growth. Our results provide novel insights into the cross talk among TFH, tumor cells, and Tregs in FL, and offer potential targets for development of therapeutic strategies to overcome immune evasion. |Blotting, Western [MESH] |Cell Separation [MESH] |Chemokine CCL17/immunology/metabolism [MESH] |Chemokine CCL22/immunology/metabolism [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Flow Cytometry [MESH] |Gene Knockdown Techniques [MESH] |Humans [MESH] |Immunohistochemistry [MESH] |Kaplan-Meier Estimate [MESH] |Lymphoma, Follicular/*immunology/metabolism/mortality [MESH] |Oligonucleotide Array Sequence Analysis [MESH] |RNA, Small Interfering [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Receptor Cross-Talk/*immunology [MESH] |T-Lymphocytes, Helper-Inducer/*immunology [MESH] |Tumor Escape/*immunology [MESH]Cross talk between follicular Th cells and tumor cells in human follic(epmc).pdf DeepDyve Pubget Overpricing