Soumission #4860 | université de toulouse – les universités et grandes écoles de toulouse midi-pyrénées
Soumission #4860 | Université de Toulouse – Les universités e.
http://www.univ-toulouse.fr/node/4163/submission/4860?sid. Votre saisie a été effectuée Vous pouvez télécharger (onglet : download PDF) et enregistrer le formulaire pour l'imprimer et collecter la signature et le cachet du directeur du laboratoire. Le document signé doit être nommé "ED_LABO_nom_prenom_resume" et envoyé scanné à [email protected] accompagné éventuellement du second fichier PDF nommé "ED_LABO_nom_prenom_detail" Votre proposition sera validée par un accusé de réception. La date limite d'envoi est fixée au 20 septembre 2012. Soumission #4860 Title of the thesis : Role of estrogen receptor (ER) alpha-signaling in regulatory T cel s on the protective action of estradiol in CNS autoimmunity Thesis supervisor : Dr Jean-Charles Guéry, PhD, DR2 INSERM e-mail address : [email protected] PhD school name : Biology, Health and Biotechnologies (BSB) Research laboratory : CPTP, INSERM U1043, CNRS U5282 Laboratory website : http://www.cptp.inserm.fr Subject short description : Clinical remissions in multiple sclerosis (MS) patients are frequently observed during pregnancy suggesting that steroid hormones, particularly estrogens, could be protective. Indeed, administration of estrogen (17ß-estradiol, E2) inhibits experimental autoimmune encephalomyelitis (EAE) in mice, the animal model of MS. We recently showed that E2-mediated inhibition of encephalitogenic T cel priming and EAE protection was dependent on estrogen receptor ! (ER!) expression in the hematopoietic compartment. Using tissue-specific ER!KO mouse models, we demonstrated that ER!-signaling in T lymphocytes, but not myeloid cel s, was required for sustained EAE protection. The goal of this proposal is now to investigate whether E2 act directly in vivo on encephalitogenic Th1/Th17 cel s or indirectly on regulatory T lymphocytes or their precursors to promote their capacity to inhibit pathogenic CD4+ T cel responses through a trans-acting mechanism of suppression. To achieve this goal we wil develop new models of ER! mutant mice, including mice selectively ER! in Foxp3+ T cel s. This project wil help to understand the pathophysiological mechanisms implicated in the modulation of MS by female sexual hormones and may lead to new therapeutic strategies. Scientific domain : Immunology Two major publications in the domain of PhD : Lélu K, Laffont S, Delpy L, Paulet PE, Périnat T, Tschanz SA, Pel etier L, Engelhardt B, and Guéry JC. Estrogen receptor !-signaling in T lymphocytes is required for estradiol- mediated inhibition of Th1 and Th17 cel differentiation and protection against EAE. J. Immunol. 2011 Sep 1;187(5):2386-93.
Lélu K, Delpy L, Robert V, Foulon E, Laffont S, Pel etier L, Engelhardt B, Guéry JC. Endogenous estrogens, through estrogen receptor !, constrain autoimmune inflammationin female mice by limiting CD4+ T-cel homing into the CNS. Eur J Immunol. 2010Dec;40(12):3489-98.
Physician Pharmaceutical Review (PPR) Case Study Jurisdiction : Florida PRIUM Case ID : Review Date : 02/04/2010 The patient is a 64-year-old female who has a long history of chronic low back pain with a date of industrial injury on 08/15/92. According to her treating physician there are multiple non-related medical issues for which he is treating her. As late as 2009 her pain
Loops permit us to execute a sequence They differ in how the repetition is Compute the average of n values entered by the user. The number of values (n) wil be specified by n = input('Enter the number of values: ');counter = 0; total = 0;while (counter < n ) total = total + x; counter = counter + 1;endif (n > 0) avg = total / counter; disp(['The average is ' num2str(avg)]);endC
