Izcue, A., Coombes, J.L. & Powrie, F. Regulatory lymphocytes and intestinal inflammation. Annu. Rev. Immunol. 27, 313-338
Sir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE, UK. Annual Review of Immunology
(Impact Factor: 39.33).
02/2009; 27:313-38. DOI: 10.1146/annurev.immunol.021908.132657
The immune system is pivotal in mediating the interactions between host and microbiota that shape the intestinal environment. Intestinal homeostasis arises from a highly dynamic balance between host protective immunity and regulatory mechanisms. This regulation is achieved by a number of cell populations acting through a set of shared regulatory pathways. In this review, we summarize the main lymphocyte subsets controlling immune responsiveness in the gut and their mechanisms of control, which involve maintenance of intestinal barrier function and suppression of chronic inflammation. CD4(+)Foxp3(+) T cells play a nonredundant role in the maintenance of intestinal homeostasis through IL-10- and TGF-beta-dependent mechanisms. Their activity is complemented by other T and B lymphocytes. Because breakdown in immune regulatory networks in the intestine leads to chronic inflammatory diseases of the gut, such as inflammatory bowel disease and celiac disease, regulatory lymphocytes are an attractive target for therapies of intestinal inflammation.
Available from: Tanedjeu Kemgang Sonfack
- "Mammals have developed an extremely sophisticated adaptive immune system of both systemic and mucosal (local) type. The immune properties of the digestive mucosa are provided by the GALT (gut-associated lymphoid tissue), composed of lymphoid aggregates, including the Peyer's patches (located mainly in the small intestinal distal ileum), where induction of immune response occurs, and mesenteric lymphoid nodes (Izcue et al. 2009). The mucosal immune system also consists of physical (mucus), molecular (antimicrobial proteins) and cellular components that act synergistically to prevent microbes from invading the body. "
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ABSTRACT: The mechanism by which probiotic lactobacilli affect the immune system is strain specific. As the immune system is multi-compartmental system, each strain has his way to interact with it and induce a visible and quantifiable effect. This review summarises the interplay existing between the host immune system, with emphasis on lactobacilli as a prototype probiotic genus. Several aspects including the bacterial-host cross-talk with the mucosal and systemic immune system are presented, as well as short sections on the competing effect toward pathogenic bacteria and their uses as delivery vehicle for antigens.This article is protected by copyright. All rights reserved.
Journal of Applied Microbiology 08/2014; 117(2):303-319. DOI:10.1111/jam.12521 · 2.48 Impact Factor
Available from: Toshiya Tanaka
- "The intestinal tract is the largest surface organ of the human body which is constantly exposed to dietary and environmental antigens such as commensal bacteria. Therefore, the intestinal immune system has to maintain homeostasis through the cooperation of various regulatory mechanisms that prevent overreaction against beneficial flora and food antigens12. Dysregulation of intestinal immune responses is believed to cause inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis, metabolic diseases such as obesity and diabetes, and is also linked to autoimmune disease34. "
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ABSTRACT: Macrophages are important for maintaining intestinal immune homeostasis. Here, we show that PPARβ/δ (peroxisome proliferator-activated receptor β/δ) directly regulates CD300a in macrophages that express the immunoreceptor tyrosine based-inhibitory motif (ITIM)-containing receptor. In mice lacking CD300a, high-fat diet (HFD) causes chronic intestinal inflammation with low numbers of intestinal lymph capillaries and dramatically expanded mesenteric lymph nodes. As a result, these mice exhibit triglyceride malabsorption and reduced body weight gain on HFD. Peritoneal macrophages from Cd300a-/- mice on HFD are classically M1 activated. Activation of toll-like receptor 4 (TLR4)/MyD88 signaling by lipopolysaccharide (LPS) results in prolonged IL-6 secretion in Cd300a-/- macrophages. Bone marrow transplantation confirmed that the phenotype originates from CD300a deficiency in leucocytes. These results identify CD300a-mediated inhibitory signaling in macrophages as a critical regulator of intestinal immune homeostasis.
Scientific Reports 06/2014; 4:5412. DOI:10.1038/srep05412 · 5.58 Impact Factor
Available from: PubMed Central
- "The immune system is pivotal in mediating interactions between the host and the microbiota that shape the intestinal environment [5,6]. Furthermore, dendritic cells (DCs) are pivotal in tolerance induction and direct the differentiation of T cells in the intestine. "
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This study investigates the effect of glucose on the LPS-induced apoptosis of dendritic cells in the intestinal tract of mice and the dendritic cell line DC2.4.
Flow cytometry was used to detect dendritic cell apoptosis both in vivo and in vitro. Hoechst 33258 staining was used to detect the morphological changes characteristic of apoptotic nuclei. Expression of apoptosis related proteins was investigated by western blot analysis and immunohistochemistry.
Pretreatment with a high concentration of glucose increased apoptosis of LPS-treated dendritic cells both in vivo and in vitro at 24 h. No effect was evident at the earlier time points of 15 min and 6 h in vitro. Furthermore, at 24 hours the expression of the survival proteins AKT, ERK and Bcl-2 was decreased, while the expression of the proapoptotic protein Bax was increased. AKT, ERK, Bcl-2 and Bax were mainly located in the cytoplasm by immunohistochemistry.
These results suggest that high glucose concentrations might prime dendritic cells for apoptosis induced by LPS in the intestinal tract through upregulating the expression of Bax and downregulating the expression of AKT, ERK and Bcl-2. Therefore, this study may give clues to understanding the immunological mechanism behind gastrointestinal complications in diabetes mellitus.
BMC Gastroenterology 05/2014; 14(1):98. DOI:10.1186/1471-230X-14-98 · 2.37 Impact Factor
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