Retraction: Regulation of Class II Expression in Monocytic Cells after HIV-1 Infection

Rakoff-Nahoum, Seth; Chen, Houchu; Kraus, Thomas; George, Ilena C.; Oei, Erwin; Tyorkin, Max; Salik, Erez; Beuria, Prarthana; Sperber, Kirk

doi:10.4049/jimmunol.177.9.6561

Cited by 1 publication

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“…Although mild‐to‐moderate intestinal inflammation occurs in the colon of mice raised under germ‐free conditions, full pathology is dependent of the presence of components of the normal microbiota. IL‐10 deficient mice do not develop intestinal inflammation in the absence of gut microbiota,40 or if MyD88, involved in TLR signaling, is concomitantly impaired 41. IL‐10 seems to act by the induction of transforming growth factor (TGF)‐β secretion in the lamina propria T cells42 as well as by p38 mitogen‐activated protein kinase (MAPK) signaling in IECs 43…”

Section: The Normal Gut Is a Noninflammatory Environmentmentioning

confidence: 99%

Host‐bacteria interactions in the intestine: homeostasis to chronic inflammation

Barbosa

Rescigno

2010

WIREs Mechanisms of Disease

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In the past decade it has become clear that the gut constitutes an important frontier of the body, which not only regulates the selective entry of nutrients while keeping vigilant against pathogens but also is largely responsible for shaping the immune response to educate the organism to recognize self from non-self. The very notion of self has undergone a dramatic change, with the acknowledgment that our 'selves' include a plethora of microbial species that actively participate in our body's homeostasis. The immune system continuously adapts to the microbiota in a cyclic, dynamic cross talk where intestinal epithelial cells play an important role in instructing noninflammatory responses for a steady-state control of bacterial growth, or triggering inflammatory mechanisms that can clear the gut from harmful invaders. The system is complex and robust in the sense that many players with partially overlapping roles act to keep the integrity of the intestinal mucosal barrier. Failure of these mechanisms involves genetic and environmental triggers and leads to inflammatory bowel disease. In this review, we seek to collect the state-of-the-art knowledge about how host and microbiota interact to promote gut homeostasis and provide evidences of malfunctioning of the described mechanisms in human inflammatory bowel disease.

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