Diminution of Circulating CD4+CD25high T Cells in Naïve Crohn’s Disease

Chamouard, P.; Monneaux, Fanny; Richert, Z.; Voegeli, Anne‐Claire; Lavaux, Thomas; Gaub, Marie Pierre; Baumann, René; Oudet, P; Muller, Sylviane

doi:10.1007/s10620-008-0590-6

Cited by 23 publications

(18 citation statements)

References 34 publications

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“…Indeed, CD4 þ and CD8 þ T-cell increase in PP was observed in a mouse model for CD and an increase in both CD4 þ and CD8 þ T cells was reported in patients with active CD, whereas the Treg population was lowered. [45][46][47] Also, the combination of smoke-induced apoptosis with other proapoptotic factors, such as the proinflammatory cytokine TNF-a, can account for a misbalance between immune defence and tolerance. 48 Once this imbalance reaches a threshold, tolerance to oral antigens is lost, resulting in an uncontrolled immune response and intestinal inflammation.…”

Section: Smoking Alters Intestinal Apoptosis and Galtmentioning

confidence: 99%

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Verschuere

Bracke

Demoor

et al. 2011

Laboratory Investigation

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Smokers have a twofold increased risk to develop Crohn's disease (CD). However, little is known about the mechanisms through which smoking affects CD pathogenesis. Especially Crohn's ileitis is negatively influenced by smoking. Interestingly, the ileum and, more in particular, the Peyer's patches in the terminal ileum are also the sites where the first CD lesions are found. Several chemokines are implicated in the pathogenesis, among which is the CCL20-CCR6 pathway. Here, we studied the gut-associated lymphoid tissue in C57BL/6 wild-type mice and in CCR6-deficient mice after exposure to air or cigarette smoke for 24 weeks. Apoptotic index of the follicle-associated epithelium overlying the Peyer's patches was evaluated. We found that chronic smoke exposure induced apoptosis in the follicle-associated epithelium. Furthermore, immune cell numbers and differentiation along with chemokine expression were determined in Peyer's patches. Important changes in immune cell composition were observed: total dendritic cells, CD4 þ T cells (including regulatory T cells) and CD8 þ T cells increased significantly after smoke exposure. The CD11b þ dendritic cell subset almost doubled. Interestingly, these changes were accompanied by an upregulated mRNA expression of the chemokines CCL9 and CCL20. However, no differences in the increase of dendritic cells were observed between wild-type and CCR6-deficient mice. Our results show that cigarette smoke exposure increases apoptosis in the follicle-associated epithelium and is associated with immune cell accumulation in Peyer's patches.

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Section: Smoking Alters Intestinal Apoptosis and Galtmentioning

confidence: 99%

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Verschuere

Bracke

Demoor

et al. 2011

Laboratory Investigation

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“…Pioneering studies by Powrie and colleagues demonstrated that the pathology in a mouse model of T cell-induced colitis, which mimics human inflammatory bowel disease (IBD), can be prevented by adoptive transfer of Foxp3 þ Treg (4). The number of Treg is lower in the peripheral blood of patients with active IBD than in that of control subjects (5). Conversely, the number of Treg is higher in the intestinal mucosa of patients with IBD, and their function is normal, as demonstrated by their ability to suppress the proliferation of effector cells in vitro (6,7).…”

Section: Introductionmentioning

confidence: 99%

Transient Ablation of Regulatory T cells Improves Antitumor Immunity in Colitis-Associated Colon Cancer

et al. 2014

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“…However, these cells were lacking in the peripheral blood of patients with the active disease, when compared to those who were in the inactive phase or in the control group [83–85]. For Tregs to be functional, a signal made by TGF- β is needed.…”

Section: T Regulatory Cellsmentioning

confidence: 99%

The Immunological Basis of Inflammatory Bowel Disease

Silva

Rodrigues

Ayrizono

et al. 2016

Gastroenterology Research and Practice

135

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Inflammatory bowel diseases (IBDs) are chronic ailments, Crohn's disease and ulcerative colitis being the most important. These diseases present an inflammatory profile and they differ according to pathophysiology, the affected area in the gastrointestinal tract, and the depth of the inflammation in the intestinal wall. The immune characteristics of IBD arise from abnormal responses of the innate and adaptive immune system. The number of Th17 cells increases in the peripheral blood of IBD patients, while Treg cells decrease, suggesting that the Th17/Treg proportion plays an important role in the development and maintenance of inflammation. The purpose of this review was to determine the current state of knowledge on the immunological basis of IBD. Many studies have shown the need for further explanation of the development and maintenance of the inflammatory process.

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Diminution of Circulating CD4+CD25high T Cells in Naïve Crohn’s Disease

Cited by 23 publications

References 34 publications

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Transient Ablation of Regulatory T cells Improves Antitumor Immunity in Colitis-Associated Colon Cancer

The Immunological Basis of Inflammatory Bowel Disease

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