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Journal articles on the topic "Immune reponse"

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Jonker, M. A., Y. Sano, A. Heneghan, J. Hermsen, and K. Kudsk. "P099 PARENTERAL NUTRITION ELIMINATES SMALL INTESTINE MUCOSAL IMMUNE REPONSE TO INJURY." Clinical Nutrition Supplements 4, no. 2 (January 2009): 67. http://dx.doi.org/10.1016/s1744-1161(09)70149-8.

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Corrêa, R. B., M. Puccioni-Sohler, S. A. P. Novis, M. S. P. Oliveira, and M. S. M. Carvalho. "5-04-06 Profile of cellular immune reponse among HAM/TSP patients in Rio de Janeiro." Journal of the Neurological Sciences 150 (September 1997): S277. http://dx.doi.org/10.1016/s0022-510x(97)86229-6.

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Khalil, Maged, Zili He, Ashish Sangal, Aref Agheli, Alka Arora, Theresa Dumlao, Seema Naik, Elizabeth Chiu, Madhumati Kalavar, and William Steier. "High Dose Glucocorticoids Potentiate the Reponse to Erythropoietin." Blood 108, no. 11 (November 16, 2006): 3775. http://dx.doi.org/10.1182/blood.v108.11.3775.3775.

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Abstract Introduction: The role of steroids in mammalian erythropoiesis has remained not well defined. At our institution, we have observed cases in which it appears that there is a synergism between Erythropoietin factor and glucocorticoids. In three cases, the patients were being treated for anemia that was slow to respond to erythropoietin, but then had a sudden quick rise in Hemoglobin following concomitant therapy with Glucocorticoids. Case #1 is a 32 year-old black female, with SLE for more than 20 years, lupus nephropathy, end-stage renal disease on maintenance Hemodialysis, for the last 5 years, chronic anemia secondary to renal failure, and thrombocytopenia due to lupus. The patient was treated with prednisone 20 mg daily as a maintenance therapy for her SLE and erythropoietin (procrit) 10,000 units injection three times a week, during each session of hemodialysis. On April 27th patient was switched over from prednisone 20mg daily to dexamethasone 6mg orally every 12 hours for 4 does followed by prednisone 40 mg orally every day for worsening thrombocytopenia. A robust rise in hemoglobin level was noticed, from 7.5gm/dl to 17.5 gm/dl within a month from the date started on high dose glucocorticoids a long with procrit. Complete work up for secondary polycythemia was all negative. Procrit was discontinued while prednisone 40mg/day was continued, hemoglobin level decreased to 14.8 g/dl, and platelet count remain stable above 150/CMM. Case #2. A 52 years old female who was diagnosed with stage 111B NSCLC treated with chemo radiation. During the period of chemo radiation hemoglobin level remained between 9–10gm/dl on procrit 40,000 units once per week. Before completion of the Chemotherapy patient developed brain metastasis treated with whole brain irradiation, Dexamethasone 4mg every 6 hours and Dilantin 100mg orally daily for seizure prophylaxis. Three weeks after starting dexamethasone hemoglobin level increased to 17 gm/dl without any obvious reason. Complete work up for secondary polycythemia was all negative. Case #3. is a 42 year old female, with HIV/AIDS (CD4<20) not on any HAART medications, Chronic anemia treated with procrit 10,000 units three times a week for six months and Feso4 325 mg tablets three times a day with hemoglobin base line around 8.00 gm/dl and Seizure. Was admitted on 12/28/05 with odynophagia, cough and shortness of breath was treated for oropharyngeal candidiasis and PCP pneumonia with Bactrim IV, Nystatin, Diflucan and Methylprednisolone 125 IV daily on 12/28/06 changed later to Prednisone 20mg orally once daily from 12/30/06 until 1/27/06. While the patient on both Glucocorticoids and procrit we notice the increased of hemoglobin from 7.7 gm/dl on 12/29/05 to 12gm/dl on 1/27/06. All other causes of secondary polycythemia have been ruled out. Conclusion: The reason for the inordinate rise in hemoglobin after starting corticosteriods could be explained by the action of corticosteriods on an immune component of the anemia, to a synergistic effect with erythropoietin on erythropoiesis through a shared mechanism or to a coincidental factor(s) unrelated to either drugs. Whatever the mechanism, When corticosteriods are prescribed for patient on erythropoietin they should be closely monitored for the development of erythrocytosis. Cautious use of glucocorticoids should be considered in patients who are refractory to erythropoietin.
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Purow, Benjamin. "Repurposing existing agents as adjunct therapies for glioblastoma." Neuro-Oncology Practice 3, no. 3 (September 30, 2015): 154–63. http://dx.doi.org/10.1093/nop/npv041.

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AbstractNumerous non-oncologic medications have been found in the last decade to have anti-cancer properties. While the focus in oncology research should clearly remain on deriving new therapeutic strategies, repurposing these existing medications may offer the potential to rapidly enhance the effectiveness of treatment for resistant cancers. Glioblastoma, the most common and lethal brain cancer, is highly resistant to standard therapies and would benefit from even minor improvements in treatment. Numerous agents already in the clinic for non-cancer applications have been found to also possess potential against cancer or specifically against glioblastoma. These include agents with activities affecting oxidative stress, the immune reponse, epigenetic modifiers, cancer cell metabolism, and angiogenesis and invasiveness. This review serves as a guide for potential ways to repurpose individual drugs alongside standard glioblastoma therapies.
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Siolas, Despina, Jane Cullis, Antonina Avanzi, Kate Byrne, Lawrence P. Leichman, Robert H. Vonderheide, and Dafna Bar-Sagi. "Antitumor activity and immune reponse in CD40 immunotherapy with gemcitabine and nab-paclitaxel in an orthotopic pancreatic cancer mouse model." Journal of Clinical Oncology 34, no. 4_suppl (February 1, 2016): 271. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.271.

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271 Background: Pancreatic cancer is well known for its aggressive clinical course and resistance to chemotherapy. A Phase I trial of CD40 immunotherapy in combination with gemcitabine demonstrated the combination was safe and achieves tumor responses in patients with pancreatic ductal adenocarcinoma. We investigated the effectiveness of gemcitabine, albumin-bound paclitaxel and CD40 agonist immunotherapy in an orthotopic pancreatic mouse model. Methods: Pancreatic cells obtained from a KrasG12D;Trp53R172H (KPC) genetically engineered mouse were cultivated in cell culture and surgically implanted into the pancreata of immunocompetent syngeneic C57/Bl6 mice allowing for tumor formation in situ. Two weeks after KPC cell implantation, mice were treated with 120 mg/kg gemcitabine and 120 mg/kg nab-paclitaxel by intraperitoneal injection. Forty eight hours after chemotherapy administration, mice were treated with 100 ug of FGK45 CD40 immunotherapy. Mouse tumors and spleens were harvested from euthanized mice ten days after drug treatment. Tumor and spleens were analyzed histologically and by flow cytometry. Results: Mice treated with combination chemotherapy and immunotherapy had a significant reduction in tumor volume in comparison to vehicle treated mice. Combination chemotherapy did not cause a significant decrease in tumor volume. No changes were seen in stromal remodeling using trichrome histological staining. Mice treated with CD40 immunotherapy had an increase in spleen size indicating an immune response. Histological and flow cytometry analysis revealed an increase in CD45+ cells in the tumors of the CD40 immunotherapy treated samples in comparison to chemotherapy alone. Conclusions: CD40 immunotherapy in combination with gemcitabine and albumin-bound paclitaxel has significant antitumor activity in an orthotopic pancreatic cancer mouse model provoking an immune response in the tumors. Future experiments will focus on identifying immune mediators critical for drug efficacy.
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Hessel, L., A. Garbarg-Chenon, J. L. Fontaine, G. Lasfargues, H. F. Clark, S. Plotkin, and F. Bricout. "Etude de la reponse immune au vaccin rotavirus vivant attenue, souche WC3, chez des enfants de 2 A 12 mois." Médecine et Maladies Infectieuses 19, no. 11 (November 1989): 627. http://dx.doi.org/10.1016/s0399-077x(89)80071-x.

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Lechner, Franziska, John Sullivan, Hans Spiegel, Douglas F. Nixon, Belinda Ferrari, Andrew Davis, Bill Borkowsky, et al. "Why do cytotoxic T lymphocytes fail to eliminate hepatitis C virus? Lessons from studies using major histocompatibility complex class I peptide tetramers." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1400 (August 29, 2000): 1085–92. http://dx.doi.org/10.1098/rstb.2000.0646.

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Hepatitis C virus (HCV) infection is a major public health problem, affecting an estimated 3% of the world's population, and over 10% in some countries. Infection in most cases becomes persistent, and can lead to hepatic inflammation, fibrosis and liver failure. The T lymphocyte reponse, in particular that mediated by cytotoxic T lymphocytes (CTLs), is likely to be involved in determining the outcome of infection, although its overall role is not clear. The use of major histocompatibility complex (MHC) class I peptide tetrameric complexes (tetramers) to study antiviral CTL responses has revolutionized our approach to the study of human infection. We have used a panel of MHC class I tetramers to analyse immune responses in HCV–infected individuals at various stages of disease. We find that the CTL response against HCV is vigorous in its early phases but dwindles over time both in terms of lymphocyte number and function. A number of potential explanations for this ‘CTL failure’ are discussed.
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Boussoffara, Thouraya, Mohamed Samir Boubaker, Melika Ben Ahmed, Mourad Mokni, Ikram Guizani, Afif Ben Salah, and Hechmi Louzir. "Histological and immunological differences between zoonotic cutaneous leishmaniasis due to Leishmania major and sporadic cutaneous leishmaniasis due to Leishmania infantum." Parasite 26 (2019): 9. http://dx.doi.org/10.1051/parasite/2019007.

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Lesion features in cutaneous leishmaniasis (CL) depend on the infecting Leishmania species as well as on host immune reponse. In this study, we evaluated the histological and immunological differences between two forms of CL described in Tunisia: zoonotic cutaneous leishmaniasis (ZCL) caused by L. major and sporadic cutaneous leishmaniasis (SCL) caused by L. infantum. Histological analysis showed a mild to moderate infiltrate within ZCL lesions. In contrast, massive infiltration of the dermis was observed within SCL lesions. Contrary to ZCL, infiltrates within SCL lesions were organized and showed granuloma composed of macrophages and lymphocytes. In addition, immunohistochemical analysis showed a predominance of CD4+ T cells within both CL forms. Furthermore, expression of interferon-γ, interleukin (IL)-10, IL-8, IL-13 and monocyte chemotactic protein (MCP)-1 was evaluated using real-time quantitative polymerase chain reaction (RT-qPCR). MCP-1 and IL-10 were expressed at comparable levels in ZCL and SCL lesions. Interestingly, IL-8 mRNA levels were significantly higher in ZCL lesions compared to SCL lesions, but interferon-γ was significantly higher in SCL lesions than in ZCL lesions.
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Pratiwi, Rahma Indah, Jusak Nugraha, Betty Agustina Tambunan, and Francisca Srioetami Tanoerahardjo. "Respons Sitokin TNF-Α Dan Il-4 Pasca Stimulasi Antigen Fusi Resat-6-CFP-10." Buletin Penelitian Kesehatan 46, no. 1 (July 4, 2018): 53–60. http://dx.doi.org/10.22435/bpk.v46i1.57.

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AbstractProtective immunity of tuberculosis (TB) infection is highly dependent on the balance of Th1 and Th2cytokines. TNF-α cytokines produced by Th1 cell retain a latent status, and IL-4 produced by Th2 aidsin the production of antibodies. The recent development of the vaccine candidates shows that rESAT-6-CFP-10 fusion antigen is specific to induce protective immune responses. The objective of the study wasto determine the immune response. This study used a quasi experimental design in the laboratory in vitrowith cultured PBMC of patients with new cases of pulmonary TB, latent TB and healthy individuals.Examination of TNF-α and IL-4 levels was done by ELISA. The highest TNF-α mean levels were 866,05in the latent TB group, compared to 814,56 in active TB and 414,58 in healthy individuals, but they werenot significantly different. The highest IL-4 mean levels were 1,39 in the active TB group, compared to0,88 in latent TB and 0,74 in healthy individuals, but they were not significantly different. High levels ofTNF-α and low levels of Il-4 in latent TB post-stimulation of rESAT-6-CFP-10 fusion antigen show thatthe candidate vaccine is capable of providing protective reponse against Mycobacterium tuberculosisinfection.Key words : TNF-α, IL-4, PBMC, ELISA, rESAT-6-CFP-10 AbstrakImunitas protektif terhadap infeksi tuberculosis sangat bergantung terhadap keseimbangan sitokinT-helper (Th)-1 dan Th2. Sitokin TNF-α yang disekresi oleh sel Th1 mampu mempertahankan status laten,dan IL-4 yang disekresi oleh Th2 membantu produksi antibodi. Pengembangan kandidat vaksin terbaruyaitu antigen fusi rESAT-6-CFP-10 bersifat spesifik terhadap respons imun protektif. Tujuan penelitianini untuk mengetahui respons imun seluler melalui kadar TNF-α dan IL-4 pasca stimulasi antigen fusirESAT-6-CFP-10. Penelitian ini menggunakan desain eksperimen semu di laboratorium secara in vitropada kultur PBMC. Pemeriksaan kadar sitokin TNF-α dan IL-4 dengan metode ELISA. Rerata kadarTNF-α pasca stimulasi paling tinggi ditemukan pada kelompok TB laten 866,05, dibandingkan TBaktif 814,56 dan orang sehat 414,58, tetapi tidak berbeda bermakna. Reratakadar IL-4 pasca stimulasipaling tinggi ditemukan pada kelompok TB aktif, dibandingkan TB laten dan orang sehat, tetapi tidakberbeda bermakna. Kadar TNF-α yang tinggi dan kadar IL-4 yang rendah pada TB laten pasca stimulasiantigen fusi rESAT-6-CFP-10 menunjukkan bahwa kandidat vaksin mampu memberikan repons protektifterhadap infeksi Mycobacterium tuberculosis secara invitro.Kata kunci : TNF-α, IL-4, PBMC, ELISA, rESAT-6-CFP-10.
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Ghanmi, Z., M. Rouabhia, O. Othmane, and P. A. Deschaux. "5.3 Effects of metal ions on cyprinid fish immune response: in vitro effects of Zn2+ and Mn2+ on the mitogenic reponse of carp pronephros lymphocytes." Developmental & Comparative Immunology 13, no. 4 (September 1989): 398. http://dx.doi.org/10.1016/0145-305x(89)90115-8.

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Dissertations / Theses on the topic "Immune reponse"

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Gibb, Alison L. "Studies on human complement component C4." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358680.

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HOUSSEAU, FRANCK. "Etude de la reponse immune cellulaire specifique des tumeurs vesicales." Paris 7, 1997. http://www.theses.fr/1997PA077042.

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L'etude du repertoire des lymphocytes t infiltrant les tumeurs (til) urotheliales primitives a mis en evidence l'existence d'expansions oligo/monoclonales pouvant refleter la stimulation d'une reponse immune au sein de la tumeur. Nous avons donc recherche, au sein des lymphocytes t infiltrant les tumeurs urotheliales, des lymphocytes t cytotoxiques (ctl) cd3/cd8 presentant une activite cytotoxique antitumorale dependante du complexe majeur d'histocompatibilite (cmh) de classe i. Nous avons etabli 5 couples constitues de til et des lignees tumorales autologues, a partir de 40 prelevements tumoraux. Quatre lignees de til lysent la lignee tumorale analogue. La caracterisation fonctionnelle de populations oligo/monoclonales cd3/cd8, isolees a partir des til d'un des patients, a demontre qu'il existe au sein des tumeurs urotheliales des ctl specifiques des cellules neoplasiques et actifs in vitro. La sous-unite beta de l'hormone chorionique gonadotrope humaine (hcg beta), produite par des tumeurs d'origines histologiques diverses, represente une cible antigenique potentielle de ces ctl. En effet, nous montrons qu'il existe en peripherie un repertoire t capable de reconnaitre cet antigene et qu'une lignee de ctl induite in vitro par des stimulations des cellules mononucleees du sang peripherique (pbmc), a l'aide d'un peptide mimant la sequence de l'hcg beta se liant a la molecule hla-a2. 1, est capable de lyser des lignees cellulaires de carcinomes urotheliaux. Ce resultat indique qu'un analogue du peptide synthetique serait genere et apprete par les cellules tumorales, a partir de la degradation de l'hcgbeta endogene, et que ce determinant antigenique serait la cible de ctl anti-tumoraux actives. L'ensemble de ces resultats montrent que les tumeurs vesicales pourraient etre les cibles d'immunotherapies specifiques des tumeurs basees sur l'utilisation d'antigenes associes a ces neoplasies.
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Dangles, Virginie. "Etude de la reponse immune cellulaire dirigee contre les tumeurs vesicales et influence de leur conformation spaciale sur l'apoptose, l'expression genique et la reponse immune." Paris 7, 2000. http://www.theses.fr/2000PA077251.

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Le cancer de la vessie est une des localisations qui beneficient d'une immunotherapie non specifique. Cependant, il est necessaire de rechercher des therapies innovantes pour les malades ne repondant pas aux traitements actuels. Dans ce cadre, nous avons etudie si la sous-unite beta de l'hormone chorionique gonadotrope humaine (hcgbeta) est un antigene capable d'induire le rejet de tumeurs. L'hcgbeta est un bon candidat : surexpression dans environ 50% des cancers vesicaux, changement d'un acide amine de l'hcgbeta lors de la transformation maligne des tumeurs vesicales et reponse peripherique contre l'hcgbeta chez un tiers des patients avec un cancer vesical producteur d'hcgbeta. Deux peptides mimant les regions 40-48 et 75-84 ont conduit a la selection de deux lignees de lymphocytes t cytotoxiques (ctl). Ces ctl sont capables de lyser des cellules de carcinomes urotheliaux. Ces resultats suggerent que des peptides derives de l'hcgbeta endogene seraient appretes et presentes par les cellules tumorales et pourraient donc servir en immunotherapie specifique des cancers de vessie. Les essais d'immunotherapie anticancereuse ont montre une frequente inadequation entre les reponses cliniques et les resultats obtenus in vitro. Le caractere tridimensionnel (3d) des tumeurs solides in vivo n'est souvent pas considere dans les systemes d'etude in vitro. Nous avons alors etudie l'influence de la conformation spatiale des cellules tumorales urotheliales sur les reponses biologiques et immunologiques. Nous avons montre que l'epidermal growth factor a des effets diametralement opposes vis a vis de l'apoptose selon que les cibles sont sous forme de tapis cellulaire (2d) ou de spheroides (3d). Nous avons ensuite demontre que l'architecture tumorale avait une forte influence sur l'activation de ctl diriges contre les cellules tumorales urotheliales : les cellules en 3d activent beaucoup moins les ctl que les cellules en 2d. Enfin, nous avons montre un effet majeur de l'architecture tumorale sur l'expression de genes codant des molecules impliquees dans l'oncogenese. L'ensemble de ces resultats demontre que l'architecture tumorale est un facteur important susceptible de modifier fortement la stimulation et la reponse du systeme immunitaire, qui doit etre pris en compte in vitro dans l'etude des antigenes de tumeurs.
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Arkwright, P. D. "Effects of the human trophoblast on lymphocyte proliferation." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236250.

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Caligiuri, Giuseppina. "La reponse immune dans l'atherosclerose et dans les syndromes coronaires aigus." Paris 7, 2000. http://www.theses.fr/2000PA077028.

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Le systeme immun est implique dans le processus d'atherogenese depuis la formation des premieres lesions (stries lipidiques), durant l'evolution vers la plaque fibreuse atheromateuse et jusqu'aux complications de plaques et leurs manifestations cliniques (syndromes coronaires aigus). La presente etude a explore le role de l'immunite specifique en relation avec l'instabilite clinique de l'atherosclerose coronaire a la fois chez l'homme et chez la souris hypercholesterolemique. Une reponse immune systemique est detectable chez les patients presentant des manifestations cliniques d'atherosclerose coronaire. Les marqueurs d'activation immunitaire sont eleves de facon constante chez les sujets souffrant d'angor stable mais ils augmentent de facon transitoire et exacerbee. Chez les patients avec angor instable et refractaires aux traitements, la reponse immune est limitee et probablement dirigee contre des antigenes presents dans les lesions coupables. En revanche, chez les patients avec angor instable sensibles aux traitements, la reponse immune est plus heterogene et moins prononcee. La souris hypercholesterolemique a ete choisie pour etudier la reponse immune dans l'atherosclerose experimentale. En fait, les souris hypercholesterolemiques males et femelles developpent une reponse immune specifique liee a l'atherosclerose et la modulation du systeme immun modifie la progression de la maladie. En particulier, le compartiment immun de la rate exerce un role protecteur. La protection est assuree par les lymphocytes b et elle est associee a une reponse contre les lipoproteines modifiee. Nous avons aussi montre que la souris hypercholesterolemique represente un modele d'infarctus aigu du myocarde. Ce modele peut donc etre utilise
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Bobé, Pierre. "La gestation : un modele d'etude de la regulation de la reponse immunitaire." Paris 7, 1987. http://www.theses.fr/1987PA077192.

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CHRISTOPHE, SYLVIE. "Approche experimentale de la reponse immune contre les hormones gonadotropes et leurs recepteurs." Paris 6, 1994. http://www.theses.fr/1994PA066837.

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Les hormones luteotrope (lh), folliculotrope (fsh) et chorionique gonadotrope (cg) appartiennent a une meme famille d'hormones glycoproteiques et sont formees par l'association non covalente de deux sous-unites distinctes alpha et beta. Elles interagissent sur des recepteurs glycoproteiques membranaires specifiques localises sur des cellules cibles presentes au niveau des gonades. Les hormones gonadotropes jouent un role cle dans le controle des processus de differenciation/proliferation des cellules ovariennes et testiculaires. Plusieurs observations cliniques suggerent que certaines infertilites masculines et feminines pourraient etre dues et/ou associees a une rupture de la tolerance immunitaire aux gonadotropines. Dans ce travail, nous avons tout d'abord resume les connaissances actuelles sur les hormones gonadotropes et leurs recepteurs ainsi que sur les processus autoimmuns impliquant ces molecules. Sur le plan experimental, notre etude a ete divisee en deux parties. Tout d'abord, nous avons analyse les phenomenes de reconnaissance immunologique de l'hcg dans un modele murin. Les processus de degradation de l'antigene generant les determinants antigeniques dans la cellule presentatrice d'antigene ont ete etudies et nous avons montre que la dissociation des sous-unites au sein d'une proteine oligomerique est une condition necessaire pour permettre l'exposition de certains determinants. La deuxieme partie de ce travail a ete consacree a l'obtention d'outils necessaires a l'etude du recepteur humain pour la hfsh car ce recepteur pourrait constituer une cible potentielle pour certains processus autoimmuns. Nous avons donc developpe un systeme de production de recepteur recombinant hfsh en cellules d'insecte. La proteine obtenue montre des caracteristiques, en terme d'affinite et de specificite de liaison, semblables a celles presentees par le recepteur produit physiologiquement. Enfin, nous avons produit et caracterise des anticorps monoclonaux diriges contre ce recepteur en utilisant une strategie basee sur l'utilisation de peptides synthetiques. Les implications cliniques et fondamentales de ce travail sont analysees.
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ASTOUL, EMMANUELLE. "Influence d'un superantigene atypique, le superantigene de la rage, sur l'induction d'une reponse immune specifique." Paris 7, 1996. http://www.theses.fr/1996PA077162.

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La nucleocapside du virus de la rage est un superantigene (sag) qui active les lymphocytes t-v8 chez l'homme, et les lymphocytes t-v6 chez la souris. Nous avons cherche a etudier l'influence de ce sag sur l'induction d'une reponse immune specifique d'un antigene heterologue. Pour cela, nous avons choisi comme modele une preparation vaccinale d'influenza, que nous avons utilisee seule ou associee au sag. La reponse immune specifique d'influenza a ete suivie chez deux souches de souris congeniques: balb/c et balb. D2, qui expriment ou non la sous-population lymphocytaire activee par le sag, la famille des lymphocytes t-v6. Nous avons observe que, chez les souris balb/c co-injectees avec influenza + le sag rabique, tous les parametres de la reponse specifique testes etaient augmentes (proliferation, secretion de cytokines, anticorps, etablissement de la reponse memoire). Cet effet n'est pas observe chez les souris balb. D2, qui ne possedent pas de lymphocytes t-v6. De plus, chez les souris balb/c, nous avons mis en evidence une augmentation preferentielle des lymphocytes t specifiques d'influenza parmi la sous-population t-v6. Ces donnees nous permettent de conclure que, de facon surprenante, 1) le sag rabique peut etre considere comme un adjuvant et 2) que cette caracteristique, necessitant la presence de lymphocytes t-v6, est liee a ses proprietes de sag. Nous avons ensuite cherche a caracteriser l'activation induite par le sag rabique, en absence d'antigene. Dans des cultures de lymphocytes issus d'amygdales humaines, nous avons compares l'effet du sag rabique a ceux de deux sag bacteriens, see et tsst-1. Nous avons observe que chez la majorite des donneurs, le sag rabique et see induisent une production d'il4 superieure a celle de tsst-1 et une production d'il2 inferieure. Le sag rabique se differenciait cependant nettement de see par l'absence totale de secretion d'ifn. L'activation lymphocytaire qu'il induit se traduit par la secretion d'igg seule, a la difference des autres sag qui provoquent la secretion d'igg et d'igm. En conclusion, le sag rabique semble favoriser la secretion de cytokines de type t2 par les lymphocytes qu'il active, et stimuler preferentiellement des lymphocytes b differencies. Le sag rabique possede donc des proprietes originales au sein de la famille deja heterogene des sag. Dans ce travail, nous discutons l'hypothese que ces caracteristiques fonctionnelles soient liees a la faible affinite qu'aurait le sag rabique pour le complexe molecules du cmh de classe ii/recepteur t
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THIAM, KADER. "Strategie de modulation de la reponse immune : du vecteur vivant au lipopeptide synthetique (doctorat : immunologie parasitologie)." Lille 2, 1999. http://www.theses.fr/1999LIL2T004.

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WACHSMANN, LEVY DOMINIQUE. "Immunite des muqueuses : etude de la reponse immune locale apres stimulation orale par des antigenes proteiques et polysaccharidiques de streptococcus mutans." Strasbourg 1, 1986. http://www.theses.fr/1986STR13125.

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Books on the topic "Immune reponse"

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Miami Bio/Technology Winter Symposium (1990 Miami, Fla.). Advances in gene technology: The molecular biology of immune diseases and the immune reponse : proceedings of the 1990 Miami Bio/Technology Winter Symposia. Oxford: IRL Press, 1990.

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Early, Eavan. Characterisation of newborn T-lymphocyte function. Dublin: University College Dublin, 1996.

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Prostaglandins, leukotrienes, and the immune response. Cambridge, [England]: Cambridge University Press, 1988.

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International Conference on Lymphocyte Activation and Immune Regulation (3rd 1990 Newport Beach, Calif.). Mechanisms of lymphocyte activation and immune regulation III: Developmental biology of lymphocytes. New York: Plenum Press, 1991.

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5

Tsutomu, Sugahara, Sagan Leonard A, and Aoyama Takashi, eds. Low dose irradiation and biological defense mechanisms: Proceedings of the International Conference on Low Dose Irradiation and Biological Defense Mechanisms, Kyoto, Japan, 12-16 July 1992. Amsterdam: Excerta Medica, 1992.

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6

Henri, Atlan, and Cohen Irun R, eds. Theories of immune networks. Berlin: Springer-Verlag, 1989.

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7

Mechanisms of Lymphocyte Activation and Immune Regulation:Vol. 2. Springer, 1989.

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8

Ninnemann, John L. Prostaglandins, Leukotrienes, and the Immune Response. Cambridge University Press, 2006.

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9

(Editor), Sudhir Gupta, William E. Paul (Editor), Max D. Cooper (Editor), and Ellen V. Rothenberg (Editor), eds. Mechanisms of Lymphocyte Activation and Immune Regulation III (Advances in Experimental Medicine and Biology). Springer, 1991.

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10

M, Snapper Clifford, ed. Cytokine regulation of humoral immunity: Basic and clinical aspects. Chichester: J. Wiley, 1996.

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