2013
DOI: 10.1016/j.cyto.2013.06.019
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Cited by 3 publications
(8 citation statements)
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“…It was found that the miR-17-92 cluster's increasing role in regulating the immune system is involved in innate and adaptive immunity, including B cells and subsets of T cells such as Th1, Th2, T follicular helper cells, regulatory T cells, monocytes/macrophages, NK cells, and dendritic cells [46]. Moreover, the study found that the miR-17 approximately 92 cluster is a critical regulator of T cell-dependent antibody responses and follicular helper T cells' (TFH cells) differentiation [47].…”
Section: T Cell Follicular Helper T Cells (Tfh Cells) and Th17mentioning
confidence: 99%
“…It was found that the miR-17-92 cluster's increasing role in regulating the immune system is involved in innate and adaptive immunity, including B cells and subsets of T cells such as Th1, Th2, T follicular helper cells, regulatory T cells, monocytes/macrophages, NK cells, and dendritic cells [46]. Moreover, the study found that the miR-17 approximately 92 cluster is a critical regulator of T cell-dependent antibody responses and follicular helper T cells' (TFH cells) differentiation [47].…”
Section: T Cell Follicular Helper T Cells (Tfh Cells) and Th17mentioning
confidence: 99%
“…Studies of global miRNA depletion in GC B and T cell-specific models showed that miRNAs are essential for proper GC formation (9,10). Dicer-mediated miRNA depletion after AID expression in early activated GC B cells impaired the production of high-affinity class-switched antibodies and the generation of memory B and long-lived plasma cells after T cell-dependent immunization due to defects in B cell proliferation and survival (9).…”
Section: Mirnas In Physiological Gc Regulationmentioning
confidence: 99%
“…Dicer-mediated miRNA depletion after AID expression in early activated GC B cells impaired the production of high-affinity class-switched antibodies and the generation of memory B and long-lived plasma cells after T cell-dependent immunization due to defects in B cell proliferation and survival (9). Likewise, DGCR8-Drosha complex-mediated miRNA depletion in CD4 T cells showed that CD4 T cell-expressed miRNAs are essential for the differentiation of Tfh cells and the induction of GC B cells during T cell-dependent immunizations (10). Interestingly, miRNAs are not only required to regulate Tfh and GC B cell function in a cell intrinsic manner, but are also important contact-independent mediators of T-B cellular communication (Figure 1).…”
Section: Mirnas In Physiological Gc Regulationmentioning
confidence: 99%
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