6 research outputs found

    Frequency of CD4<sup>+</sup> T-cell subsets in the peripheral blood of patients with ulcerative colitis in <i>sustained clinical remission</i>.

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    <p>PBMCs were isolated from heparinized blood samples from patients treated with mesalazine or a herbal preparation at baseline and 1, 3, 6, 9, and 12 month after baseline. The expression of CD4, CD25, and intracellular Foxp3 as determined by flow cytometry is shown as the percentage of indicated T-cell subsets under mesalazine treatment (A) or herbal preparation treatment (B) per patient (gray). Mean value per time point is shown in black.</p

    Regulatory function of CD4<sup>+</sup>CD25<sup>high</sup> T cells during remission and clinical flare.

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    <p>PBMCs from healthy donors and from patients with ulcerative colitis were stained for CD4 and CD25 expression. CD4<sup>+</sup>CD25<sup>−</sup> and CD4<sup>+</sup>CD25<sup>hgh</sup> regulatory T cells were sorted by flow cytometry. (A) Gating strategy and purity of sorted CD4<sup>+</sup>CD25<sup>−</sup> and CD4<sup>+</sup>CD25<sup>high</sup> cells are demonstrated as dot plot. (B) CD4<sup>+</sup>CD25<sup>−</sup> responder T cells were co-cultured at a ratio of 2 to 1 with or without autologous CD4<sup>+</sup>CD25<sup>hgh</sup> regulatory T cells under stimulation with Treg suppression inspector beads. The proliferation of responder cells was measured by the loss of CFSE dye, and inhibition was calculated.</p

    Frequency of CD4<sup>+</sup> T-cell subsets in the peripheral blood of patients with ulcerative colitis experiencing <i>a clinical flare</i>.

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    <p>PBMCs were isolated from heparinized blood samples from patients with ulcerative colitis treated with mesalazine (A) or herbal preparation (B) at indicated time points. The expression of CD4, CD25, and intracellular Foxp3 was determined by flow cytometry. Results are demonstrated as kinetic per patient (gray). Mean value per time point is shown in black.</p

    Demographic data and pre-study clinical characteristics for the two treatment methods (mesalazine and herbal preparation) and the healthy control group.

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    <p>ns = not significant.</p><p>*E1 Ulcerative proctitis: Involvement limited to the rectum (that is, proximal extent of inflammation is distal to the rectosigmoid junction). E2 Left-sided UC (distal UC): Involvement limited to a portion of the colorectum distal to the splenic flexure. E3 Extensive UC (pancolitis): Involvement extends proximal to the splenic flexure.</p

    Baseline frequency of CD4<sup>+</sup> T-cell subsets in the peripheral blood of patients with ulcerative colitis in remission and healthy donors as determined by flow cytometry for the expression of CD4 and CD25 and intracellular Foxp3.

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    <p>(A) Gating strategy for CD4 and CD25 expression is shown as a dot plot. Expression of Foxp3 by indicated CD4<sup>+</sup> T cell subsets demonstrated as histograms. (B) Baseline percentage of indicated T-cell subsets among CD4<sup>+</sup> T cells in healthy controls and patients with ulcerative colitis in remission before treatment with mesalazine or herbal preparation. Means are shown as scatter plot. Mean values are indicated by lines.</p

    Epithelial colonization by gut dendritic cells promotes their functional diversification.

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    Dendritic cells (DCs) patrol tissues and transport antigens to lymph nodes to initiate adaptive immune responses. Within tissues, DCs constitute a complex cell population composed of distinct subsets that can exhibit different activation states and functions. How tissue-specific cues orchestrate DC diversification remains elusive. Here, we show that the small intestine included two pools of cDC2s originating from common pre-DC precursors: (1) lamina propria (LP) CD103+CD11b+ cDC2s that were mature-like proinflammatory cells and (2) intraepithelial cDC2s that exhibited an immature-like phenotype as well as tolerogenic properties. These phenotypes resulted from the action of food-derived retinoic acid (ATRA), which enhanced actomyosin contractility and promoted LP cDC2 transmigration into the epithelium. There, cDC2s were imprinted by environmental cues, including ATRA itself and the mucus component Muc2. Hence, by reaching distinct subtissular niches, DCs can exist as immature and mature cells within the same tissue, revealing an additional mechanism of DC functional diversification
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