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Letteratura scientifica selezionata sul tema "Immunity"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 9 novembre 2024

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Articoli di riviste sul tema "Immunity"

DH, Jha. "Immunity and Ayurveda". Journal of Natural & Ayurvedic Medicine 4, n. 2 (2 aprile 2020): 1. http://dx.doi.org/10.23880/jonam-16000248.

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&NA;. "Immunity lost, immunity regained". Inpharma Weekly &NA;, n. 760 (ottobre 1990): 17. http://dx.doi.org/10.2165/00128413-199007600-00049.

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Khudhair, Abdulkareem Salman. "Herd Immunity or Community Immunity". Scholars Journal of Medical Case Reports 08, n. 04 (30 aprile 2020): 508–9. http://dx.doi.org/10.36347/sjmcr.2020.v08i04.026.

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Cotter, S. C., e R. M. Kilner. "Personal immunity versus social immunity". Behavioral Ecology 21, n. 4 (4 giugno 2010): 663–68. http://dx.doi.org/10.1093/beheco/arq070.

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Takahashi, Hidemi. "Innate Immunity and Acqired Immunity". Journal of Nippon Medical School 69, n. 5 (2002): 410–14. http://dx.doi.org/10.1272/jnms.69.410.

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Lee, Theodore M. "Immunity". Emerging Infectious Diseases 22, n. 4 (aprile 2016): 766. http://dx.doi.org/10.3201/eid2204.151858.

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Wilkinson, Lise. "Immunity". Lancet 365, n. 9469 (aprile 2005): 1459. http://dx.doi.org/10.1016/s0140-6736(05)66405-7.

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Reddy, Karthik, Moritz Schularick e Vasiliki Skreta. "IMMUNITY". International Economic Review 61, n. 2 (31 marzo 2020): 531–64. http://dx.doi.org/10.1111/iere.12433.

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Muske, Carol. "Immunity". Missouri Review 9, n. 1 (1985): 20–21. http://dx.doi.org/10.1353/mis.1985.0140.

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Lewin, Benjamin. "Immunity". Immunity 1, n. 1 (aprile 1994): 1. http://dx.doi.org/10.1016/1074-7613(94)90002-7.

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Più fonti

Tesi sul tema "Immunity"

Daneshvar, Fatemeh. "L’immunité juridictionnelle des États et des organismes d'État". Thesis, Université de Lorraine, 2018. http://www.theses.fr/2018LORR0270.

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L'immunité juridictionnelle des États a été pendant des siècles une question incontestée fondée sur le principe de l'égalité des Etats et sur leur indépendance absolue. Cette règle a été élaborée à une époque où tenter une action contre un État dans un pays étranger aurait été considéré comme une violation de sa souveraineté. Toutefois, les fonctions des Etats ont changé au cours des siècles. Désormais, les Etats s’engagent dans les activités commerciales comme une personne privée et jouent un rôle essentiel dans ce secteur.Alors, bien que le droit de l'immunité soit lié à l'octroi de l'immunité aux États pour leur permettre d'accomplir efficacement les fonctions publiques, le droit international moderne n'exige pas que les tribunaux d'un Etat s’abstiennent de connaître un litige simplement parce que l’État étranger n'a pas la volonté de défendre.Ce travail de recherche, est donc consacré à l’étude de l’immunité de juridiction et l’immunité d’exécution afin de montrer le droit international actuel sur la matière.Cette thèse vise à examiner une question spécifique qui a été mise en évidence au cours de ces dernières années. Comment et dans quelle mesure les États et ses démembrements devraient être soumis à des règles spécifiques de l'immunité d’Etat ?
The issue of jurisdictional immunity of states was for centuries an undisputed matter based on the principle of state equality and absolute independence of states. The rules were developed at a time when it was thought to be an infringement of a state's sovereignty to bring proceedings against it or its officials in a foreign country. However, the functions of states have changed over the centuries and nowadays states are involved in commercial activities as a private person and accordingly play an essential role in the commercial activities of the world. In fact, the issue of state immunities is an increasingly important and rapidly developing area of international law and practice. The state practice reflects the emerging global consensus that States and State enterprises can no longer claim absolute, unrestrained immunity from the proper jurisdiction of foreign courts, especially for their commercial activities. Therefore, although the law of state immunity is related to the grant of immunities to states to enable them to carry out their public functions effectively, modern international law does not require the courts of one state to refrain from deciding a case merely because a foreign state is an unwilling defendant. It is therefore important to know how a plea of state immunity may be made and to what type of dispute it applies

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Alculumbre, Solana. "Division of Labor Between Distinct Human Plasmacytoid Dendritic Cell Subsets Following Viral Activation". Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS014.

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L’existence d’un partage des tâches a été démontrée au sein de nombreux systèmes biologiques et ce notamment en immunologie où il a été décrit dans le contexte de différentes sous-populations d’un même type cellulaire. Les cellules dendritiques plasmacytoïdes (pDC) jouent un rôle clé lors des infections virales. Les pDCs ont la capacité de sécréter de grandes quantités d’interférons de type I et de se différencier en cellules dendritiques matures capables d’activer une réponse immunitaire adaptative. Il a été proposé que ces fonctions innées et adaptatives soient séquentiellement induites après activation virale. Au cours de ma thèse, je me suis intéressée à ces deux fonctions principales des pDC et je suis arrivée à la description de différentes sous-populations de pDC activées : PD-L1+CD80- (P1), PD-L1+CD80+ (P2) and PD-L1-CD80+ (P3), démontrant qu’il existe un partage des tâches entre ces sous-types. P1 produit spécifiquement de l’IFN-α, indiquant une spécialisation en immunité innée, et promeut une réponse tolérogénique des cellules T CD4. Inversement, P3 induit une forte activation des cellules T CD4 naïves et une polarisation de type Th2, démontrant une spécialisation fonctionnelle dans l’immunité adaptative. P2 possède un profil fonctionnel intermédiaire. Plutôt qu’un lien séquentiel, nos résultats indiquent une exclusion réciproque des fonctions innées et adaptatives entre ces différents sous-types de pDC
Under microbial stimulation plasmacytoid pre-dendritic cells (pDC) secrete large amounts of type I interferon (IFN) and differentiate into mature dendritic cells capable of activating T cells. These innate and adaptive functions are thought to be induced sequentially in pDC through triggering of the IRF-7 and NFkB pathways, respectively. We found that viral activation of pDC induced their differentiation into three phenotypically distinct subsets: PD-L1+CD80- (P1), PD-L1+CD80+ (P2) and PD-L1-CD80+ (P3). P1 specifically produced IFN-α, indicating a specialization in innate immunity, while promoting weak activation and high IL-10 expression in CD4 T cells. Conversely, P3 showed increased expression of surface costimulatory molecules, improved migratory capacity, strong naïve CD4 T cell activation, and induction of Th2 differentiation. P2 had an intermediate functional profile. No conversion could be induced between subsets. We identified P1 in psoriatic skin, and blood from active lupus patients. Our results indicate reciprocal exclusion, rather than sequential link, of innate and adaptive pDC functions, with important implications in immune regulation and immunopathology

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Zunino, Barbara. "Dialogue entre le métabolisme et l’immunité dans le traitement des cancers". Thesis, Nice, 2014. http://www.theses.fr/2014NICE4113.

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Il est connu depuis de nombreuses années que le métabolisme des cellules cancéreuses diffère de celui des cellules saines. La Restriction Calorique (RC) est connue pour prolonger la durée de vie et pour limiter l’oncogenèse. Ainsi, il a été montré que la RC et ses mimétiques comme le 2-deoxyglucose (2DG) augmentent l’efficacité de la chimiothérapie et peuvent aussi induire une immunité anti-tumorale. J’ai pu montrer qu’en régulant le métabolisme via la restriction calorique (ou des mimétiques) nous pouvions moduler l’expression de la protéine anti-apoptotique Mcl-1. Ainsi nous avons établi in vivo et in vitro que la RC restaure la sensibilité des cellules de lymphome à l’apoptose induite par un inhibiteur de Bcl-2/XL, l’ABT-737. Nous avons aussi établi que ces effets sont indépendants de la protéine p53 et/ou des « protéines BH3-only ». La deuxième partie de mon travail a été d’élucider les mécanismes moléculaires mis en place lors de la Chimiothérapie Hyperthermique Intra péritonéale (CHIP) pouvant expliquer les effets bénéfiques observés chez les patients atteints d’une carcinose péritonéale (CP). Une partie de ces bénéfices sont dus à la mise en place d’une immunité anti-tumorale. En utilisant des modèles in vivo et in vitro j’ai mis en évidence l’implication de la protéine du choc thermique 90 (Hsp90) dans l’effet observé. Ainsi, l’inhibition spécifique de la Hsp90 réverse les effets protecteurs de la CHIP, soulignant l’importance de cette protéine dans notre modèle d’immunité anti-tumorale
The link between cell metabolism and cancer at the cellular level has long been known. Caloric restriction (CR) is known to prolong lifespan and to protect from cancer incidence. The molecular mechanisms involved in these benefic effects have been evaluated and may offer new opportunities for therapeutic intervention. Moreover, CR and CR-mimetics such as 2-deoxyglucose (2DG) has been shown to enhance chemotherapy efficiency and to induce an anti-cancer immune response. During the period of my PhD I demonstrated how the modulation of metabolism through caloric restriction or through its mimetics could significantly reduce the expression of the anti-apoptotic protein Mcl-1 and sensitize lymphoma-bearing mice to apoptosis induced by a Bcl-2/XL inhibitor, ABT-737. We have demonstrated that CR can control Mcl-1 translation and sensitize cells to ABT-737-induced death regardless of the presence or absence of p53 and/or of the main “BH3-only proteins”. Then, I focused on deciphering the molecular mechanisms allowing the Hyper-thermic Intra-Peritoneal Chemotherapy (HIPEC) to be beneficial to patients suffering from peritoneal carcinomatosis. Part of the protective effect was mediated through the induction of an efficient anti-cancer immune response. Next, I showed the involvement of heat shock proteins 90 (Hsp90) in the observed effect. Indeed, when Hsp90 was blocked we lost the protection induced by the HIPEC-treated cells, therefore underling the role of Hsp90 in this HIPEC-dependent induction of anti-cancer immune response

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Champiat, Stéphane. "Caractérisation clinique et biologique de l’hyperprogression tumorale lors du blocage de la voie PD-1/PD-L1". Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS040.

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Les anticorps bloquant les points de contrôle immunitaires modifient profondément la gestion des patients atteints de cancer. À la pointe de cette nouvelle classe d'agents anticancéreux, les anticorps anti-PD-1 / PD-L1 peuvent ainsi restaurer une réponse efficace des cellules T antitumorales. En conséquence, ces agents sont maintenant approuvés dans divers types de tumeurs, tels que le mélanome, le cancer bronchique non à petites cellules, le cancer du rein, les tumeurs ORL ou le cancer de la vessie. Ces nouvelles immunothérapies entraînent également de nouveaux profils de réponse tumorale tels que des réponses tumorales retardées ou des pseudoprogressions. Au fil de l’expérience acquise avec ces traitements, il a été observé chez certains patients un état de progression rapide de la maladie, ce qui pourrait suggérer que le blocage de points de contrôle immunitaire pourrait avoir un effet délétère en accélérant la maladie chez un sous-groupe de patients. Ce travail de thèse a permis de caractériser sur le plan clinique et biologique ce phénomène d’accélération de la croissance tumorale sous immunothérapie anti-checkpoint que nous avons définit “maladie hyperprogressive” (HPD). L’analyse transcriptomique d’échantillons tumoraux de ces patients a permis d’orienter vers un rôle spécifique de l’environnement myeloide
Immune checkpoint blocking antibodies are profoundly changing the management of patients with cancer. At the forefront of this novel anticancer agent class, anti-PD-1/PD-L1 antibodies can exhibit a significant activity by restoring an efficient antitumor T-cell response. As a result, these agents are now approved in various tumor types such as melanoma, squamous, and nonsquamous non–small cell lung cancer (NSCLC), renal cell carcinoma (RCC), head and neck squamous cell carcinoma (HNSCC) or bladder cancer. Interestingly, these new immunotherapies also result in novel tumor response patterns such as delayed tumor responses or pseudoprogressions. As experience grows with these therapeutics, anecdotal reports are relating rapid disease progressions, which could suggest that immune checkpoint blockade may have a deleterious effect by accelerating the disease in a subset of patients. This thesis work has made it possible to characterize clinically and biologically this phenomenon of accelerated tumor growth under anti-checkpoint immunotherapy, which we have defined as “hyperprogressive disease” (HPD). Transcriptomic analysis of tumour samples from these patients suggested a specific role for the myeloid environment

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Yates, Philip John. "Immunity to paramyxoviruses". Thesis, Open University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262218.

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Yang, Lili Rothenberg Ellen V. "Towards engineering immunity /". Diss., Pasadena, Calif. : California Institute of Technology, 2004. http://resolver.caltech.edu/CaltechETD:etd-06042004-000641.

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Zunino, Barbara. "Dialogue entre le métabolisme et l’immunité dans le traitement des cancers". Electronic Thesis or Diss., Nice, 2014. http://www.theses.fr/2014NICE4113.

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Walker, Lee Charles. "Foreign State Immunity & Foreign Official Immunity: The Human Rights Dimension". Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/18198.

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This thesis concerns the attempt to establish human rights exceptions to foreign state immunity. The problem has multiple facets. Firstly, suits against foreign governments should be distinguished from suits against foreign officials. Further, in the latter context there is a distinction both between criminal and civil cases and between cases against individuals with immunity ratione personae and those with immunity ratione materiae. Individuals suffering extraterritorial jus cogens violations have been increasingly seeking justice against foreign governments and officials. Restrictive immunity largely displaced absolute immunity in the Western and developing world during the latter half of the Twentieth Century. This restrictive immunity only retained immunity for acta jure imperii. Many common-law nations entered into treaties and enacted foreign state immunity legislation purportedly embodying the restrictive doctrine, but these treaties and statutes actually accord a complete immunity to foreign states, subject only to specific, enumerated exceptions. Drafted mostly from the 1960s to the 1980s, they are to some extent from a bygone era. The chief issue of the time was whether state-owned trading entities should be immune from suit. The rights of private traders were upheld with the recognition of inter alia the commercial activity exception. In modern times, the human rights or jus cogens exception is now an important battleground. Research into attempts to establish such an exception to immunity was split into: (1) the origin and history of foreign state immunity and foreign official immunity; (2) the human rights dimension to foreign state immunity; and (3) the human rights dimension to foreign official immunity. In each part, representative cases were selected to best draw out the developmental contours. To aid holistic understanding of these cases, the litigation is followed from first instance to the exhaustion of appeals. The main findings of the thesis were, in regard to: (1) it is arguable whether sufficient uniformity in practice established absolute immunity as a binding norm and, even if it did, this could only have been during 1920-1976; (2) foreign state immunity statutes were mostly drafted before human rights cases against foreign states became an issue, as such they are not designed to cope and a jus cogens amendment may be necessary; (3) the High Court of Australia has the chance to break with older UK precedent, favoured by Canada, by paying closer regard to the discussion of the US Supreme Court on the matter of whether the definition of foreign state should include a foreign official.

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Tadie, Jean Marc. "Rôles clinico-biologiques du monoxyde d'azote produit par les voies aériennes". Thesis, Paris Est, 2010. http://www.theses.fr/2010PEST0053/document.

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Le monoxyde d'azote (NO) est une molécule produite par l'ensemble des cellules des voies aériennes. Sa synthèse à partir de la L-arginine fait appel à un groupe d'enzymes : les NO synthases (NOS). Il existe trois isoformes de NOS exprimées par des cellules ayant des fonctions diverses conférant ainsi au NO produit une spécificité d'action dépendante de la cellule et de la « situation » ayant entraîné sa synthèse. Les travaux effectués dans le cadre de cette thèse explorent des rôles différents (bronchoréactivité, immunitaires) du NO produit par les voies aériennes ainsi que la mesure du NO dans le contexte de l'anesthésie – réanimation. L'objectif du premier travail était de « revisiter » la fonction régulatrice du tonus bronchique dans le cadre d'une pathologie respiratoire, l'objectif du second travail était méthodologique (étude des sources anatomiques du NO expiré chez le patient sous ventilation mécanique), et l'objectif du troisième travail était d'utiliser la mesure validée dans le second travail pour évaluer les fonctions immunes du NO en réanimation.Premier travail. La compétition entre les NO synthases et les arginases pour leur substrat commun, la L-arginine, pourrait être impliquée dans régulation de la réactivité et du remodelage bronchique chez le patient atteint de BPCO. Le but du premier travail était d'évaluer la relation entre expression de cette balance enzymatique, et les effets pharmacologiques de l'inhibition des NOS et des arginases sur la réactivité bronchique ex vivo à l'acétylcholine de patients sans et avec une BPCO peu sévère. Pour cela, nous avons étudié les bronches de 22 patients. Des études immunohistochimiques nous ont permis de mettre en évidence une expression bronchique NOS-2 plus importante chez les patients BPCO comparée aux patients non BPCO. De plus, les études pharmacologiques réalisées en cuve à organe ont permis de mettre en évidence une tension bronchique de base plus importante chez les BPCO, corrélée à l'expression de la NOS-2 et au degré d'obstruction bronchique (VEMS). L'utilisation d'inhibiteur des NOS diminuait cette tension de base. Nous avons démontré ainsi qu'une augmentation de l'expression NOS-2 chez le BPCO était impliquée dans l'augmentation du tonus bronchique de base et dans l'obstruction bronchique.Second travail. Les variations de NO expiré après chirurgie cardiaque avec circulation extracorporelle (CEC) demeurent controversées. Le but de ce deuxième travail était de déterminer quelle source de NO expiré (bronchique ou alvéolaire) était modifiée après CEC, et d'étudier les effets de la ventilation mécanique pendant la CEC sur ces variations. Nous avons étudié ainsi 32 patients ventilés ou non durant une chirurgie cardiaque avec CEC. Nous avons observé une diminution significative du NO expiré d'origine bronchique après la CEC. Cette diminution n'était pas observée lors du maintien durant la CEC d'une ventilation avec pression expiratoire positive (PEEP). Ce travaille permettait de conclure que la diminution du NO bronchique après la CEC pouvait être liée à une occlusion des petites voies aériennes. Cette atteinte de petites voies aériennes était prévenue par la PEEP.Troisième travail. Enfin, dans ce troisième travail, nous avons émis l'hypothèse que la mesure du NO produit par les voies aériennes (NO expiré et nasal) pouvait constituer un marqueur prédictif de survenue d'infection nosocomiale (fonctions immunitaires du NO). Dans une étude observationnelle chez 45 patients de réanimation ventilés (15 patients ont développé une infection nosocomiale), le NO nasal était le seul marqueur significativement plus bas chez les patients développant une infection nosocomiale (le NO expiré, les dosages d'IL6 et d'IL10 ainsi que le score SOFA n'étaient pas différents entre les deux groupes). Un NO nasal inférieur à 148 ppb 72 heures après l'admission du patient, permettait de prédire la survenue d'une infection nosocomiale avec une sensibilité et une spécificité de 80% et de 70% respectivement et un odds ratio de 2.7. Le développement de ce bio marqueur simple à mesurer permettrait de mettre en place des stratégies préventives (immunonutrition avec de la L-arginine)
In the respiratory tract, NO is produced by a wide variety of cell types and is generated via oxidation of l-arginine that is catalyzed by the enzyme NO synthase (NOS). NOS exists in three distinct isoforms: neuronal NOS (NOS-1), inducible NOS (NOS-2), and endothelial NOS (NOS-3). NO derived from the constitutive isoforms of NOS (NOS-1 and NOS-3) and other NO-adduct molecules (nitrosothiols) have been shown to be modulators of bronchomotor tone. On the other hand, NO derived from NOS-2 seems to be a proinflammatory mediator with immunomodulatory effects. This thesis explores the physiological and pathophysiological role of endogenous nitric oxide in the airways, and the clinical aspects of monitoring nitric oxide in exhaled air of patients with respiratory disease.First Study: competition between nitric oxide synthases (NOSs) and arginases for their common substrate l-arginine could be involved in the regulation of cholinergic airway reactivity and subsequent airway remodeling. The aims of this study were to evaluate the relationships between the expression of this enzymatic balance and the effects of NOS and arginase inhibition on bronchoconstrictive response to acetylcholine of patients without and with early chronic obstructive pulmonary disease (COPD). Twenty-two human bronchi were investigated for immunohistochemistry and modulation of acetylcholine-induced airway constriction. Significantly increased expression of NOS2 in immunoblots of bronchial tissue and staining in smooth muscle cells was evidenced in patients with COPD compared with control subjects. Forced expiratory volume in 1 s (FEV1) and NOS2 expression were negatively correlated. Pharmacological experiments demonstrated that resting tension was elevated in COPD compared with control subjects and was positively correlated with the expression of NOS2. The sole effect of the specific arginase inhibitor Nomega-hydroxy-nor-L-arginine was to decrease sensitivity in COPD patients, whereas NG-nitro-L-arginine methyl ester unexpectedly decreased resting tension because of a non-cGMP-dependent effect. In conclusion, an upregulation of NOS2 expression in COPD patients is involved in airway tone regulation and functional airflow limitation, whereas increased arginase activity is involved in airway sensitivity.Second Study: the change in exhaled NO after cardio-pulmonary bypass remains controversial. The aims were to determine whether exhaled NO sources (alveolar or bronchial) are modified after bypass, and whether mechanical ventilation (MV) settings during bypass modify exhaled NO changes. Thirty-two patients were divided into three groups: without MV during bypass and positive end-expiratory pressure (PEEP) (n=12), dead space MV without PEEP (n=10) and dead space MV with PEEP (n=10). Alveolar NO concentration and bronchial NO flux were calculated before and 1h after surgery using a two-compartment model of NO exchange developed in spontaneous breathing patients. Whereas a significant decrease in bronchial NO was found after bypass in the two groups without PEEP during bypass, this decrease was not observed in patients with dead space ventilation with PEEP. Alveolar NO was not significantly modified whatever the ventilation settings. In conclusion, the impairment of bronchial NO seemed related to airway closure since dead space mechanical ventilation with PEEP prevented its decrease.Third Study: the development of biomarkers able to predict the occurrence of nosocomial infection could help manage preventive strategies, especially in medical patients whose degree of acquired immunosuppression may be variable. We hypothesized that the NO fraction present in the airways (upper and lower) of critically ill patients under mechanical ventilation could constitute such a biomarker. We conducted an observational study in a medical intensive care unit. Forty-five patients (26 men; 72 [25th-75th percentiles] years [56-82]; Simplified Acute Physiology Score II, 63 [50-81], 14 infected) under mechanical ventilation (>3 days) underwent on day 1 and day 3 of their stay: nasal and exhaled (partitioned in bronchial and alveolar sources) bedside NO measurements, determination of urine NO end products and plasma cytokine (IL-6, IL-10) concentrations, and Sequential Organ Failure Assessment score calculation. Nosocomial infection incidence was recorded during the 15 subsequent days. Fifteen patients (33%) acquired a nosocomial infection. Nasal NO was the only marker significantly different between patients with and without subsequent infection (day 1, 52 ppb [20-142] vs. 134 [84-203], P = 0.038; day 3, 98 ppb [22-140] vs. 225 [89-288], P = 0.006, respectively). Nasal NO fraction 148 ppb or less at day 3 had an 80% sensitivity, a 70% specificity, and an odds ratio of 2.7 (95% confidence interval, 1.9-3.8) to predict acquisition of nosocomial infection. Nasal NO seems to be a relatively sensitive and specific biomarker of subsequent nosocomial infection acquisition

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Catozzi, Carlotta. "Water buffalo microbiota and immunity during infectious diseases". Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670193.

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La tesi té com a objectiu investigar la resposta immune dels búfals d’aigua (Bubalus bubalis) durant malalties infeccioses (per exemple, mastitis, brucel·losi i tuberculosi) i malalties de produccions, com malalties metabòliques relacionades amb el peripart o l’estrès. Tenint en compte la relació entre l’entorn microbià i el sistema immunitari, també s’ha identificat el contingut de la microbiota de llet. El sistema immunitari del búfalo d’aigua ha estat poc caracteritzat fins ara, per no parlar de la microbiota, que era desconeguda. Els búfals d’aigua són sensibles a les mateixes malalties que els remugants, com per exemple mastitis, tuberculosi, brucel·losi, però no es coneix l’impacte d’aquestes malalties sobre el sistema immune dels búfals. El búfal d’aigua presenta diferències anatòmiques (per exemple a la glàndula mamària i a nivell de la pell) i fisiològiques (malalties infeccioses i periparts) en comparació amb els remugants. Per tant, és evident que tant el sistema immune com la microbiota podrien presentar diverses diferències. A la meva tesi doctoral vaig tractar d’abordar algunes d’aquestes qüestions. En primer lloc, es va investigar la microbiota de llet dels búfals d’aigua en relació amb la mastitis. En segon lloc, l’avaluació de la resposta immune, en termes d’expressió gènica i miRNAs, es va tractar en animals afectats per brucel·losi i tuberculosi. Finalment, es va realitzar la caracterització del període de transició mesurant proteïnes de fase aguda per avaluar l’estat de la inflamació durant el període de transició.
El objetivo de la tesis es investigar la respuesta inmunitaria de los búfalos de agua (Bubalus bubalis) durante las enfermedades infecciosas (por ejemplo, mastitis, brucelosis y tuberculosis) y las enfermedades de producción, como las enfermedades metabólicas relacionadas con el periparto o el estrés. Debido a que el sistema inmunitario está relacionado con el entorno microbiano, también se ha caracterizado la composición de la microbiota de la leche. Hasta el momento, el sistema inmunitario del búfalo de agua no estaba bien caracterizado y la microbiota de la leche era desconocida. Aunque los búfalos sean sensibles a las mismas enfermedades que los rumiantes (como por ejemplo mastitis, tuberculosis, brucelosis), se desconoce el impacto de estas enfermedades en el sistema inmunitario de los búfalos. En comparación con los otros rumiantes, el búfalo de agua presenta diferencias anatómicas (por ejemplo, en la glándula mamaria y en la piel) y fisiológicas (enfermedades infecciosas y peripartos). Por lo tanto, es evidente que tanto el sistema inmune como la microbiota podrían presentar varias diferencias. En mi tesis doctoral, he abordado algunos de estos problemas. En primer lugar, se investigó la microbiota de leche de los búfalos de agua durante la enfermedad de la mastitis. En segundo lugar, se evaluó la respuesta inmunitaria en animales afectados por brucelosis y tuberculosis, mediante técnicas de expresión génica y miRNAs. Finalmente, se caracterizó el período de transición midiendo las proteínas de fase aguda para evaluar el estado de inflamación.
The thesis aims to investigate the immune response of water buffaloes (Bubalus bubalis) during infectious diseases (e.g. mastitis, brucellosis and tuberculosis) and productions diseases, such as peripartum related metabolic diseases or stress. Given the relationship between the microbial environment and the immune system, the microbiota content of milk has been identified as well. The immune system of water buffalo has been poorly addressed so far, not to mention the microbiota, which was unknown. Dairy water buffaloes are sensitive to the same diseases as dairy ruminants, such as for example mastitis, tuberculosis, brucellosis, but the impact of these diseases on water buffaloes’ immune system are unknown. Water buffalo presents anatomical (e.g. at mammary gland and skin level) and physiological (peripartum and infectious diseases) differences as compared to cow and other dairy ruminants. Therefore, it is evident that both the immune system and microbiota could present several differences. In my PhD thesis, I tried to address some of these issues. Firstly, the milk microbiota of water buffaloes was investigated in relation to mastitis disease. Secondly, the evaluation of the immune response, in terms of gene expression ad miRNAs, was carried out in animals affected by brucellosis and tuberculosis. Finally, the characterization of the transition period was performed measuring acute phase proteins to assess the inflammation status during the transition period.

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Weiner, Michael A. Maximum immunity. Boston: Houghton Mifflin, 1986.

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