Institution
French Institute of Health and Medical Research
Government•Paris, France•
About: French Institute of Health and Medical Research is a government organization based out in Paris, France. It is known for research contribution in the topics: Population & Receptor. The organization has 109367 authors who have published 174236 publications receiving 8365503 citations.
Topics: Population, Receptor, Immune system, Transplantation, T cell
Papers published on a yearly basis
Papers
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TL;DR: An evolutionary basis for human elementary arithmetic is suggested by the finding that when participants viewed sets of items with a variable number, the bilateral intraparietal sulci responded selectively to number change.
969 citations
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TL;DR: Two mutations of the gene encoding the neuronal voltage-gated sodium channel (SCN1A), Thr875Met and Arg1648His, that co-segregate with the disorder in two families with GEFS+ linked to chromosome 2q are described, identifying a new disease gene for human inherited epilepsy.
Abstract: Generalized epilepsy with febrile seizures plus type 2 (GEFS+2, MIM 604233) is an autosomal dominant disorder characterized by febrile seizures in children and afebrile seizures in adults. We describe here two mutations of the gene encoding the neuronal voltage-gated sodium channel (SCN1A), Thr875Met and Arg1648His, that co-segregate with the disorder in two families with GEFS+ linked to chromosome 2q. These mutations identify a new disease gene for human inherited epilepsy.
968 citations
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TL;DR: It is shown that peptidoglycan from Gram-negative bacteria is necessary and sufficient to induce the genesis of ILFs in mice through recognition by the NOD1 (nucleotide-binding oligomerization domain containing 1) innate receptor in epithelial cells, and β-defensin 3- and CCL20-mediated signalling through the chemokine receptor CCR6.
Abstract: Isolated lymphoid follicles (ILFs) are areas of specialized lymphoid tissue found in the lining of the small intestine where they are involved in protecting the host from invading pathogens. A new study of the composition of ILFs and the factors required for their formation has found that they are induced in the mouse small intestine by the presence of peptidoglycan from Gram-negative bacteria via recognition by the NOD1 innate receptor in epithelia cells. ILFs range from clusters of a few B cells to well-organized lymphoid nodules. Once established, the ILFs exert control over the make-up of the bacterial community. This rare example of microbe-induced tissue genesis in mammals demonstrates how a constructive 'dialogue' between bacteria and host can contribute to efficient digestion and protection from intestinal pathogens. The generation of isolated lymphoid follicles is shown to depend on NOD1-induced responses to bacterial components. Isolated lymphoid follicles are in turn are shown to affect the composition of the host microbiota. Intestinal homeostasis is critical for efficient energy extraction from food and protection from pathogens. Its disruption can lead to an array of severe illnesses with major impacts on public health, such as inflammatory bowel disease characterized by self-destructive intestinal immunity. However, the mechanisms regulating the equilibrium between the large bacterial flora and the immune system remain unclear. Intestinal lymphoid tissues generate flora-reactive IgA-producing B cells, and include Peyer's patches and mesenteric lymph nodes, as well as numerous isolated lymphoid follicles (ILFs)1,2. Here we show that peptidoglycan from Gram-negative bacteria is necessary and sufficient to induce the genesis of ILFs in mice through recognition by the NOD1 (nucleotide-binding oligomerization domain containing 1) innate receptor in epithelial cells, and β-defensin 3- and CCL20-mediated signalling through the chemokine receptor CCR6. Maturation of ILFs into large B-cell clusters requires subsequent detection of bacteria by toll-like receptors. In the absence of ILFs, the composition of the intestinal bacterial community is profoundly altered. Our results demonstrate that intestinal bacterial commensals and the immune system communicate through an innate detection system to generate adaptive lymphoid tissues and maintain intestinal homeostasis.
965 citations
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TL;DR: Guided by the expression of Neurogenin 3 (Ngn3), the earliest islet cell-specific transcription factor in embryonic development, it is shown that beta cell progenitors can be activated in injured adult mouse pancreas and are located in the ductal lining.
964 citations
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TL;DR: The results clearly demonstrate that RARs are essential for vertebrate ontogenesis and therefore that retinoic acid is the active retinoid, which is required at several stages of the development of numerous tissues and organs.
Abstract: Compound null mutations of retinoic acid receptor (RAR) genes lead to lethality in utero or shortly after birth and to numerous developmental abnormalities. In the accompanying paper (Lohnes, D., Mark., M., Mendelsohn, C., Dolle, P., Dierich, A., Gorry, Ph., Gansmuller, A. and Chambon, P. (1994). Development 120, 2723-2748), we describe malformations of the head, vertebrae and limbs which, with the notable exception of the eye defects, were not observed in the offspring of vitamin A-deficient (VAD) dams. We report here abnormalities in the neck, trunk and abdominal regions of RAR double mutant mice, which include: (i) the entire respiratory tract, (ii) the heart, its outlow tract and the great vessels located near the heart, (iii) the thymus, thyroid and parathyroid glands, (iv) the diaphragm, (v) the genito-urinary system, and (vi) the lower digestive tract. A majority of these abnormalities recapitulate those observed in the fetal VAD syndrome described by Joseph Warkany's group more than fourty years ago [Wilson, J. G., Roth, C. B. and Warkany, J. (1953) Am. J. Anat., 92, 189-217; and refs therein]. Our results clearly demonstrate that RARs are essential for vertebrate ontogenesis and therefore that retinoic acid is the active retinoid, which is required at several stages of the development of numerous tissues and organs. We discuss several possibilities that may account for the apparent functional redundancy observed amongst retinoic acid receptors during embryogenesis.
963 citations
Authors
Showing all 109539 results
Name | H-index | Papers | Citations |
---|---|---|---|
Guido Kroemer | 236 | 1404 | 246571 |
Pierre Chambon | 211 | 884 | 161565 |
Peer Bork | 206 | 697 | 245427 |
Ronald M. Evans | 199 | 708 | 166722 |
Raymond J. Dolan | 196 | 919 | 138540 |
Matthew Meyerson | 194 | 553 | 243726 |
Charles A. Dinarello | 190 | 1058 | 139668 |
Julie E. Buring | 186 | 950 | 132967 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Didier Raoult | 173 | 3267 | 153016 |
Giuseppe Remuzzi | 172 | 1226 | 160440 |
Zena Werb | 168 | 473 | 122629 |
Nahum Sonenberg | 167 | 647 | 104053 |
Philippe Froguel | 166 | 820 | 118816 |
Gordon J. Freeman | 164 | 579 | 105193 |