High and Low Vitamin A Therapies Induce Distinct FoxP3+ T-Cell Subsets and Effectively Control Intestinal Inflammation

Kang, Seung Goo; Wang, Chuanwu; Matsumoto, Satoshi; Kim, Chang H.

doi:10.1053/j.gastro.2009.06.063

Cited by 82 publications

(67 citation statements)

References 38 publications

(48 reference statements)

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“…A possible reason for this finding might be that VAS improved immunity and affected the inflammatory mechanism. 21,22 This parallel effect of VAS also suggested that VAS may not damage the inherent association between URTI and diarrhea.…”

Section: Discussionmentioning

confidence: 95%

Prevalence of Diarrhea Among Children Less Than 36 Months of Age in Rural Western China in 2001 and 2005

Gao¹,

Liu²,

Yan³

2014

The American Journal of Tropical Medicine and Hygiene

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Abstract. We collected for rural western China data for 14,658 children less than 36 months of age in 2001 and for 14,112 children in 2005. A generalized estimated equation log-binomial model was used to identify the determinants of childhood diarrhea. In 2005, prevalence of diarrhea was approximately 7.4%, which compared with that for 2001, had decreased by 8.7%. The generalized estimated equation analysis showed that region affected the prevalence of childhood diarrhea significantly. Age was negatively associated with childhood diarrhea. Although childhood upper respiratory infections increased the risk of diarrhea, the risk could be decreased by use of vitamin A in the previous year. In addition, children of Han ethnicity or those living in one-child families had a lower risk of diarrhea in 2001, but underweight children had a higher risk in 2005. These findings may have some implications for formulating policies of childhood diarrhea prevention and control in rural western China.

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Section: Discussionmentioning

confidence: 95%

Prevalence of Diarrhea Among Children Less Than 36 Months of Age in Rural Western China in 2001 and 2005

Gao¹,

Liu²,

Yan³

2014

The American Journal of Tropical Medicine and Hygiene

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“…Vitamin A-deficient mice have fewer T cells in the intestinal lamina propria, supporting the importance of a vitamin A-dependent homing pathway in vivo. 197,199 …”

Section: Intestinal DC Ra and The Imprinting Of Lymphocyte Homingmentioning

confidence: 98%

Intestinal dendritic cells

Kamm

Stagg

et al. 2010

Inflammatory Bowel Diseases

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Dendritic cells (DCs) play a key role in discriminating between commensal microorganisms and potentially harmful pathogens and in maintaining the balance between tolerance and active immunity. The regulatory role of DC is of particular importance in the gut where the immune system lies in intimate contact with the highly antigenic external environment. Intestinal DC constantly survey the luminal microenvironment. They act as sentinels, acquiring antigens in peripheral tissues before migrating to secondary lymphoid organs to activate naive T cells. They are also sensors, responding to a spectrum of environmental cues by extensive differentiation or maturation. Recent studies have begun to elucidate mechanisms for functional specializations of DC in the intestine that may include the involvement of retinoic acid and transforming growth factor-β. Specialized CD103(+) intestinal DC can promote the differentiation of Foxp3(+) regulatory T cells via a retinoic acid-dependent process. Different DC outcomes are, in part, influenced by their exposure to microbial stimuli. Evidence is also emerging of the close interaction between bacteria, epithelial cells, and DC in the maintenance of intestinal immune homeostasis. Here we review recent advances of functionally specialized intestinal DC and their mechanisms of antigen uptake and recognition. We also discuss the interaction of DC with intestinal microbiota and their ability to orchestrate protective immunity and immune tolerance in the host. Lastly, we describe how DC functions are altered in intestinal inflammation and their emerging potential as a therapeutic target in inflammatory bowel disease.

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“…Moreover, RA confers gut-homing properties on the regulatory T cells (Tregs) by increasing their expression of a4b7 and CCR9 (40,54), partly through a BATF-dependent mechanism (55). In both mice and humans, RA cooperates with TGF-b to promote conversion of naive CD4 + T cells into Foxp3 + iTregs (37,53,56), and this effect is mediated, at least in part, through RARa (53,57 (58).…”

Section: Ra In Innate Immunity Including Its Influence On Apcsmentioning

confidence: 99%

Modulation of T Cell and Innate Immune Responses by Retinoic Acid

Raverdeau

Mills

2014

The Journal of Immunology

179

155

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Retinoic acid (RA) is produced by a number of cell types, including macrophages and dendritic cells, which express retinal dehydrogenases that convert vitamin A to its main biologically active metabolite, all-trans RA. All-trans RA binds to its nuclear retinoic acid receptors that are expressed in lymphoid cells and act as transcription factors to regulate cell homing and differentiation. RA production by CD103+ dendritic cells and alveolar macrophages functions with TGF-β to promote conversion of naive T cells into Foxp3+ regulatory T cells and, thereby, maintain mucosal tolerance. Furthermore, RA inhibits the differentiation of naive T cells into Th17 cells. However, Th1 and Th17 responses are constrained during vitamin A deficiency and in nuclear RA receptor α–defective mice. Furthermore, RA promotes effector T cell responses during infection or autoimmune diseases. Thus, RA plays a role in immune homeostasis in the steady-state but activates pathogenic T cells in conditions of inflammation.

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High and Low Vitamin A Therapies Induce Distinct FoxP3+ T-Cell Subsets and Effectively Control Intestinal Inflammation

Cited by 82 publications

References 38 publications

Prevalence of Diarrhea Among Children Less Than 36 Months of Age in Rural Western China in 2001 and 2005

Prevalence of Diarrhea Among Children Less Than 36 Months of Age in Rural Western China in 2001 and 2005

Intestinal dendritic cells

Modulation of T Cell and Innate Immune Responses by Retinoic Acid

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