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Beurze S.M.,Radboud University Nijmegen | Toni I.,Radboud University Nijmegen | Pisella L.,Institute National Of La Sante Et Of La Recherche Medicale | Pisella L.,University Claude Bernard Lyon 1 | Medendorp W.P.,Radboud University Nijmegen
Journal of Neurophysiology | Year: 2010

To plan a reaching movement, the brain must integrate information about the spatial goal of the reach with positional information about the selected hand. Recent monkey neurophysiological evidence suggests that a mixture of reference frames is involved in this process. Here, using 3T functional magnetic resonance imaging (fMRI), we tested the role of gaze-centered and body-centered reference frames in reach planning in the human brain. Fourteen human subjects planned and executed arm movements to memorized visual targets, while hand starting position and gaze direction were monitored and varied on a trial-by-trial basis. We further introduced a variable delay between target presentation and movement onset to dissociate cerebral preparatory activity from stimulus- and movement-related responses. By varying the position of the target and hand relative to the gaze line, we distinguished cerebral responses that increased for those movements requiring the integration of peripheral target and hand positions in a gaze-centered frame. Posterior parietal and dorsal premotor areas showed such gaze-centered integration effects. In regions closer to the primary motor cortex, body-centered hand position effects were found. These results suggest that, in humans, spatially contiguous neuronal populations operate in different frames of reference, supporting sensorimotor transformations according to gaze-centered or body-centered coordinates. The former appears suited for calculating a difference vector between target and hand location, whereas the latter may be related to the implementation of a joint-based motor command. Copyright © 2010 The American Physiological Society. Source

Fauriat C.,Institute National Of La Sante Et Of La Recherche Medicale | Olive D.,Institute National Of La Sante Et Of La Recherche Medicale
Blood | Year: 2014

In this issue of Blood, Nanbakhsh et al show that leukemic cell lines rendered resistant to cytarabine display a higher expression of the natural killer (NK) group 2, member D (NKG2D) ligands (NKG2DL) UL-16 binding proteins 1-3 (ULBP1-3). This expression is c-Myc dependent as it is abrogated by c-Myc inhibitors or small interfering RNA. Consequently, upregulation of NKG2DL renders the cell lines more sensitive to NK-cell-mediated lysis. © 2014 by The American Society of Hematology. Source

Fava V.M.,McGill University | Cobat A.,McGill University | Van Thuc N.,Hospital for Dermato Venerology | Latini A.C.P.,Lauro Of Souza Lima Institute | And 15 more authors.
Journal of Infectious Diseases | Year: 2015

Background. Type 1 reactions (T1R) affect a considerable proportion of patients with leprosy. In those with T1R, the host immune response pathologically overcompensates for the actual infectious threat, resulting in nerve damage and permanent disability. Based on the results of a genome-wide association study of leprosy per se, we investigated the TNFSF15 chromosomal region for a possible contribution to susceptibility to T1R. Methods. We performed a high-resolution association scan of the TNFSF15 locus to evaluate the association with T1R in 2 geographically and ethnically distinct populations: a family-based sample from Vietnam and a case-control sample from Brazil, comprising a total of 1768 subjects. Results. In the Vietnamese sample, 47 single-nucleotide polymorphisms (SNPs) overlapping TNFSF15 and the adjacent TNFSF8 gene were associated with T1R but not with leprosy. Of the 47 SNPs, 39 were cis-expression quantitative trait loci (cis-eQTL) for TNFSF8 including SNPs located within the TNFSF15 gene. In the Brazilian sample, 18 of these cis-eQTL SNPs overlapping the TNFSF8 gene were validated for association with T1R. Conclusions. Taken together, these results indicate TNFSF8 and not TNFSF15 as an important T1R susceptibility gene. Our data support the need for infection genetics to go beyond genes for pathogen control to explore genes involved in a commensurate host response. © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. Source

Van Maele L.,Institute Pasteur Of Lille | Van Maele L.,Institute National Of La Sante Et Of La Recherche Medicale | Van Maele L.,French National Center for Scientific Research | Van Maele L.,University of Lille Nord de France | And 39 more authors.
Journal of Infectious Diseases | Year: 2014

Mucosal sites are continuously exposed to pathogenic microorganisms and are therefore equipped to control respiratory infections. Type 3 innate lymphoid cells (ILC3) are key players in antimicrobial defense in intestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production. The present study aimed at analyzing the distribution and function of ILC3 in the respiratory tract. We first observed that lung mucosa harbors a discrete population of ILC3 expressing CD127, CD90, CCR6, and the transcriptional factor RORγt. In addition, lung ILC3 were identified as a major source of IL-22 in response to interleukin 23 stimulation. During Streptococcus pneumoniae infection, ILC3 rapidly accumulated in the lung tissue to produce IL-22. In response to S. pneumoniae, dendritic cells and MyD88, an important adaptor of innate immunity, play critical functions in IL-22 production by ILC3. Finally, administration of the Toll-like receptor 5 agonist flagellin during S. pneumoniae challenge exacerbated IL-22 production by ILC3, a process that protects against lethal infection. In conclusion, boosting lung ILC3 might represent an interesting strategy to fight respiratory bacterial infections. © The Author 2014. Source

Ouederni M.,Pediatric Hematology Immunology Unit | Ouederni M.,Tunis el Manar University | Sanal O.,Ankara University | Ikinciogullari A.,Hacettepe University | And 51 more authors.
Clinical Infectious Diseases | Year: 2014

Background. Interleukin 12Rβ1 (IL-12Rβ1)-deficient patients are prone to clinical disease caused by mycobacteria, Salmonella, and other intramacrophagic pathogens, probably because of impaired interleukin 12-dependent interferon production. About 25% of patients also display mucocutaneous candidiasis, probably owing to impaired interleukin 23-dependent interleukin 17 immunity. The clinical features and outcome of candidiasis in these patients have not been described before, to our knowledge. We report here the clinical signs of candidiasis in 35 patients with IL-12Rβ1 deficiency.Results. Most (n = 71) of the 76 episodes of candidiasis were mucocutaneous. Isolated oropharyngeal candidiasis (OPC) was the most common presentation (59 episodes, 34 patients) and was recurrent or persistent in 26 patients. Esophageal candidiasis (n = 7) was associated with proven OPC in 2 episodes, and cutaneous candidiasis (n = 2) with OPC in 1 patient, whereas isolated vulvovaginal candidiasis (VVC; n = 3) was not. Five episodes of proven invasive candidiasis were documented in 4 patients; 1 of these episodes was community acquired in the absence of any other comorbid condition. The first episode of candidiasis occurred earlier in life (median age±standard deviation, 1.5 ± 7.87 years) than infections with environmental mycobacteria (4.29 ± 11.9 years), Mycobacterium tuberculosis (4 ± 3.12 years), or Salmonella species (4.58 ± 4.17 years) or other rare infections (3 ± 11.67 years). Candidiasis was the first documented infection in 19 of the 35 patients, despite the vaccination of 10 of these 19 patients with live bacille Calmette-Guérin.Conclusions. Patients who are deficient in IL-12Rβ1 may have candidiasis, usually mucocutaneous, which is frequently recurrent or persistent. Candidiasis may be the first clinical manifestation in these patients. © The Author 2013. Source

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