Relevant bibliographies by topics / Tuberculosis immunity

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Tuberculosis immunity'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Tuberculosis immunity.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Tuberculosis immunity"

1

Triccas, James A., Nathalie Winter, Carl G. Feng, and Nicholas P. West. "Immunity toMycobacterium tuberculosis." Clinical and Developmental Immunology 2011 (2011): 1–2. http://dx.doi.org/10.1155/2011/406549.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Philips, Jennifer A., and Joel D. Ernst. "Tuberculosis Pathogenesis and Immunity." Annual Review of Pathology: Mechanisms of Disease 7, no. 1 (February 28, 2012): 353–84. http://dx.doi.org/10.1146/annurev-pathol-011811-132458.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Jacobs, Ashley, and Robert John Wilkinson. "Humoral immunity in tuberculosis." European Journal of Immunology 45, no. 3 (March 2015): 647–49. http://dx.doi.org/10.1002/eji.201570034.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

van Crevel, Reinout, Tom H. M. Ottenhoff, and Jos W. M. van der Meer. "Innate Immunity to Mycobacterium tuberculosis." Clinical Microbiology Reviews 15, no. 2 (April 2002): 294–309. http://dx.doi.org/10.1128/cmr.15.2.294-309.2002.

Full text
Abstract:
SUMMARY The different manifestations of infection with Mycobacterium tuberculosis reflect the balance between the bacillus and host defense mechanisms. Traditionally, protective immunity to tuberculosis has been ascribed to T-cell-mediated immunity, with CD4+ T cells playing a crucial role. Recent immunological and genetic studies support the long-standing notion that innate immunity is also relevant in tuberculosis. In this review, emphasis is on these natural, innate host defense mechanisms, referring to experimental data (e.g., studies in gene knockout mice) and epidemiological, immunological, and genetic studies in human tuberculosis. The first step in the innate host defense is cellular uptake of M. tuberculosis, which involves different cellular receptors and humoral factors. Toll-like receptors seem to play a crucial role in immune recognition of M. tuberculosis, which is the next step. The subsequent inflammatory response is regulated by production of pro- and anti-inflammatory cytokines and chemokines. Different natural effector mechanisms for killing of M. tuberculosis have now been identified. Finally, the innate host response is necessary for induction of adaptive immunity to M. tuberculosis. These basic mechanisms augment our understanding of disease pathogenesis and clinical course and will be of help in designing adjunctive treatment strategies.
APA, Harvard, Vancouver, ISO, and other styles
5

Martens, Gregory W., Meltem Cevik Arikan, Jinhee Lee, Fucheng Ren, Therese Vallerskog, and Hardy Kornfeld. "Hypercholesterolemia Impairs Immunity to Tuberculosis." Infection and Immunity 76, no. 8 (May 27, 2008): 3464–72. http://dx.doi.org/10.1128/iai.00037-08.

Full text
Abstract:
ABSTRACT We demonstrate that apolipoprotein E -deficient (ApoE −/ −) mice are highly susceptible to tuberculosis and that their susceptibility depends on the severity of hypercholesterolemia. Wild-type (WT) mice and ApoE −/ − mice fed a low-cholesterol (LC) or high-cholesterol (HC) diet were infected with ∼50 CFU Mycobacterium tuberculosis Erdman by aerosol. ApoE −/ − LC mice were modestly more susceptible to tuberculosis than WT LC mice. In contrast, ApoE −/ − HC mice were extremely susceptible, as evidenced by 100% mortality after 4 weeks with tuberculosis. The lung pathology of ApoE −/ − HC mice was remarkable for giant abscess-like lesions, massive infiltration by granulocytes, elevated inflammatory cytokine production, and a mean bacterial load ∼2 log units higher than that of WT HC mice. Compared to WT HC mice, the gamma interferon response of splenocytes restimulated ex vivo with M. tuberculosis culture filtrate protein was delayed in ApoE −/ − HC mice, and they failed to control M. tuberculosis growth in the lung. OT-II cells adoptively transferred into uninfected ApoE −/ − HC mice had a weak proliferative response to their antigen, indicating impaired priming of the adaptive immune response. Our studies show that ApoE −/ − deficiency is associated with delayed expression of adaptive immunity to tuberculosis caused by defective priming of the adaptive immune response and that elevated serum cholesterol is responsible for this effect.
APA, Harvard, Vancouver, ISO, and other styles
6

Dietrich, Jes, Sugata Roy, Ida Rosenkrands, Thomas Lindenstrøm, Jonathan Filskov, Erik Michael Rasmussen, Joseph Cassidy, and Peter Andersen. "Differential Influence of Nutrient-Starved Mycobacterium tuberculosis on Adaptive Immunity Results in Progressive Tuberculosis Disease and Pathology." Infection and Immunity 83, no. 12 (September 28, 2015): 4731–39. http://dx.doi.org/10.1128/iai.01055-15.

Full text
Abstract:
When infected withMycobacterium tuberculosis, most individuals will remain clinically healthy but latently infected. Latent infection has been proposed to partially involveM. tuberculosisin a nonreplicating stage, which therefore represents anM. tuberculosisphenotype that the immune system most likely will encounter during latency. It is therefore relevant to examine how this particular nonreplicating form ofM. tuberculosisinteracts with the host immune system. To study this, we first induced a state of nonreplication through prolonged nutrient starvation ofM. tuberculosisin vitro. This resulted in nonreplicating persistence even after prolonged culture in phosphate-buffered saline. Infection with either exponentially growingM. tuberculosisor nutrient-starvedM. tuberculosisresulted in similar lung CFU levels in the first phase of the infection. However, between week 3 and 6 postinfection, there was a very pronounced increase in bacterial levels and associated lung pathology in nutrient-starved-M. tuberculosis-infected mice. This was associated with a shift from CD4 T cells that coexpressed gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) or IFN-γ, TNF-α, and interleukin-2 to T cells that only expressed IFN-γ. Thus, nonreplicatingM. tuberculosisinduced through nutrient starvation promotes a bacterial form that is genetically identical to exponentially growingM. tuberculosisyet characterized by a differential impact on the immune system that may be involved in undermining host antimycobacterial immunity and facilitate increased pathology and transmission.
APA, Harvard, Vancouver, ISO, and other styles
7

Wawrocki, Sebastian, and Magdalena Druszczynska. "Inflammasomes inMycobacterium tuberculosis-Driven Immunity." Canadian Journal of Infectious Diseases and Medical Microbiology 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/2309478.

Full text
Abstract:
The development of effective innate and subsequent adaptive host immune responses is highly dependent on the production of proinflammatory cytokines that increase the activity of immune cells. The key role in this process is played by inflammasomes, multimeric protein complexes serving as a platform for caspase-1, an enzyme responsible for proteolytic cleavage of IL-1βand IL-18 precursors. Inflammasome activation, which triggers the multifaceted activity of these two proinflammatory cytokines, is a prerequisite for developing an efficient inflammatory response against pathogenicMycobacterium tuberculosis(M.tb). This review focuses on the role of NLRP3 and AIM2 inflammasomes inM.tb-driven immunity.
APA, Harvard, Vancouver, ISO, and other styles
8

Baker, R. W., A. Zumla, and G. A. W. Rook. "Tuberculosis, steroid metabolism and immunity." QJM 89, no. 5 (May 1, 1996): 387–94. http://dx.doi.org/10.1093/qjmed/89.5.387.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

McShane, Helen, and Ann Williams. "Tuberculosis vaccine promises sterilizing immunity." Nature Medicine 17, no. 10 (October 2011): 1185–86. http://dx.doi.org/10.1038/nm.2503.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Schwander, Stephan, and Keertan Dheda. "Human Lung Immunity againstMycobacterium tuberculosis." American Journal of Respiratory and Critical Care Medicine 183, no. 6 (March 15, 2011): 696–707. http://dx.doi.org/10.1164/rccm.201006-0963pp.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Tuberculosis immunity"

1

Elias, Daniel. "Helminths and immunity against tuberculosis /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-035-4/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Ronan, Edward. "Understanding vaccine induced protective immunity to Mycobacterium tuberculosis." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:c0d7b20f-e144-42f8-aa52-301d0938b0b3.

Full text
Abstract:
The current worldwide epidemic of Mycobacterium tuberculosis infection is a huge global health problem. Widespread BCG vaccination remains a useful tool in combating this epidemic; however, its variable efficacy requires urgent development of novel vaccines against Mycobacterium tuberculosis. Such a candidate vaccine is a serotype 5 adenovirus expressing antigen 85A from M. tuberculosis (Ad85A). In animal models Ad85A confers significant protection when administered intra-nasally. The work in this thesis demonstrates that intra-nasal immunisation with Ad85A results in inhibition of M. tuberculosis growth in the lung early after infection, in contrast to the late inhibition induced by parenterally administered vaccines. Early inhibition correlates with the presence in the lung of a highly activated population of antigen-specific CD8 T cells, maintained for at least 6 months post-immunisation by persistent antigen. For intra-nasal Ad85A to be effective, the vaccine must be delivered into the lower respiratory tract, as immunisation targeting only the nasal-associated lymphoid tissue (NALT) does not result in protection. Following a change of animal facility, the lung immune response to intra-dermal immunisation with Ad85A increased and this route of immunisation now induced protection, though growth of M. tuberculosis was inhibited only late after infection. However, this response and protection can be altered by exposure to environmental mycobacteria. Further experiments showed that simultaneous respiratory and parenteral immunisations (SIM) act additively, where local lung immunity inhibits the growth of M. tuberculosis early after infection and systemic immunity protects later. SIM regimes generate greatly improved protection over either immunisation alone and do not depend on priming and boosting.
APA, Harvard, Vancouver, ISO, and other styles
3

Hicks, Alice Sophie. "Defining biomarkers of protective immunity and disease for tuberculosis." Thesis, St George's, University of London, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589943.

Full text
Abstract:
Tuberculosis (TB) is still a significant global public health problem. The only current vaccine, BCG, gives variable protection, especially in adults. Several new vaccines are currently in clinical trials but no correlates of protective immunity to TB have been defined. Therefore, vaccines have to go through extensive pre-clinical assessments and clinical trials. Once identified, correlates of protection could be used as early end-points during clinical trials, reducing costs and easing the assessment of a greater number of vaccine candidates. In addition, more reliable biomarkers of TB disease are required so that measuring the effects of therapeutic interventions during drug and vaccine trials is more accurate. A genome-wide microarray was utilised to identify potential correlates of protection induced post-BCG vaccination and post-M. tuberculosis challenge, and to identify biomarkers of disease in the non-human primate model of tuberculosis. Gene expression profiles generated from peripheral blood mononuclear cells isolated during past vaccine efficacy studies were analysed in two species of macaque where the outcome of infection was known. Differentially expressed genes were identified in a series of pair-wise comparisons. Post-vaccination, no genes could be identified which were indicative of a protective immune response in both species. Six weeks post-challenge, gene expression profiles generated from animals able to control TB infection revealed an up-regulation of genes related to the Th17 response whereas animals that were unable to control infection showed up-regulation of a number of iron regulatory genes. This was further investigated at post-mortem using RT-PCR to detect iron regulatory genes in conjunction with analysis of serum iron and transferrin levels. An up- regulation of genes for ferritin, transferrin receptor, SLCllAl and SLCllA2 coupled with lower serum iron levels compared with disease controllers suggests that in animals unable to control infection, iron is redirected intracellularly where it is utilised by the mycobacteria for growth. • 4 34
APA, Harvard, Vancouver, ISO, and other styles
4

Redford, Paul Stuart. "Regulatory mechanisms inhibiting anti-mycobacterial immunity following Mycobacterium tuberculosis infection." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445023/.

Full text
Abstract:
The work reported in this thesis addresses the regulatory factors that function to limit the initiation of protective immune responses following exposure to the bacterium Mycobacterium tuberculosis (MTb). Control and clearance of intracellular pathogens, such as MTb, is dependent on the cytokine Tumour Necrosis Factor (TNF) and induction of a T-helper 1 (Thl) response, which is characterised by production of IFN-gamma driven by interleukin (IL)-12. In other infection models the presence of the immunosuppressive cytokine IL-10 in the local milieu has been shown to down-regulate Thl responses thus limiting detrimental host induced immune-pathology. To determine a role for IL-10 following murine infection, we examined its function during acute and chronic infections with two strains of H37Rv obtained from either i) National Institute for Medical Research (NIMR) or ii) London School of Hygiene and Tropical Medicine (LSHTM). IL-10 receptor blockade during the chronic phase of MTb infection reduced bacterial burdens in mice infected with H37Rv NIMR, but not mice infected with H37Rv LSHTM. However, despite the lack of effect of IL-10 blockade on the bacterial load during chronic infection with H37Rv LSHTM, immune cells obtained from MTb infected mice produced elevated levels of IFN-gamma when stimulated in vitro in the presence of IL-10 blocking antibodies. In addition, neutralisation of IL-10 before and during acute MTb infection with H37Rv LSHTM resulted in a transient reduction in bacterial burdens and enhanced IFN-gamma production, suggesting that IL-10 plays a role in regulating the early immune response to MTb. Additional regulators that may function together with or in parallel to IL-10 to limit bacterial clearance such as regulatory T cells (Tregs) have been shown to be regulators of autoimmunity, atopy and infectious disease. Using flow cytometric analysis of the Treg specific transcription factor FoxP3, we observed an early increase in the number of lung Tregs following aerosol MTb infection of mice. However, when addressing the effect on bacterial clearance in the absence of Tregs by either i) antibody depletion or ii) adoptive transfer approaches into immuno-deficient mice, a suppressive role for Tregs on bacterial burdens could not be found. Finally this work evaluated the role of plasmacytoid precursor DC (pDC) during MTb infection, which is in contrast their normal function as mediators of the anti viral response. Upon in vitro exposure to viable MTb, plasmacytoid pDC could not be infected and did not produce pro-inflammatory cytokines. Using flow cytometry, we observed no increase in plasmacytoid pDC in either the lung or spleen during the early stages of aerosol or intravenous infection. In addition, antibody depletion of plasmacytoid pDC during the early stages of MTb infection did not affect bacterial load. In summary, the data suggests that plasmacytoid pDC play only a minor role during the early immune response to MTb.
APA, Harvard, Vancouver, ISO, and other styles
5

Sutiwisesak, Rujapak. "Natural Polymorphism of Mycobacterium tuberculosis and CD8 T Cell Immunity." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1076.

Full text
Abstract:
Coevolution between Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, and the human host has been documented for thousands of years. Interestingly, while T cell immunity is crucial for host protection and survival, T cell antigens are the most conserved region of the Mtb genome. Hypothetically, Mtb adapts under immune pressure to exploit T cell responses for its benefit from inflammation and tissue destruction for ultimately transmission. EsxH, a gene encoding immunodominant TB10.4 protein, however, contains polymorphic regions corresponding to T cell epitopes. Here, I present two complementary analyses to examine how Mtb modulates TB10.4 for immune evasion. First, I use a naturally occurring esxH polymorphic clinical Mtb isolate, 667, to investigate how A10T amino acid exchange in TB10.4 affect T cell immunity. To verify and identify the cause of the immunological differences, I construct isogenic strains expressing EsxHA10T or EsxHWT. In combination with our recent finding that TB10.44-11-specific CD8 T cells do not recognize Mtb-infected macrophages, we hypothesize that TB10.4 is a decoy antigen as it distracts host immunity from inducing other potentially protective responses. I examine whether an elimination of TB10.44-11-specific CD8 T cell response leads to a better host protective immunity. The studies of in vivo infection and in vitro recognition in this dissertation aim to provide a better understanding of the counteraction between immune evasion and protective immunity.
APA, Harvard, Vancouver, ISO, and other styles
6

Temmerman, Stéphane. "Etude de la réponse à médiation cellulaire indute par l'héparin-binding hemagglutinin chez le sujet infecté par Mycobacterium tuberculosis." Doctoral thesis, Universite Libre de Bruxelles, 2004. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211117.

Full text
Abstract:
La tuberculose demeure un problème majeur de santé publique. Mycobacterium tuberculosis infecte un tiers de la population mondiale et environ 3 millions de décès, des suites de l’infection, sont recensés chaque année dans le monde. La mise au point d’une stratégie vaccinale efficace constitue dès lors la solution idéale pour tenter d’éradiquer la bactérie. Le système immunitaire humain répond à l’infection par l’induction d’une réponse cellulaire, caractérisée essentiellement par la sécrétion de médiateurs pro-inflammatoires, comme l’interféron-gamma (IFN-?). A la fois les lymphocytes T CD4+ et T CD8+ produisent cette cytokine, mais les seconds sont également doués de propriétés cytotoxiques, entraînant la mort de la cellule infectée et du bacille. L’évaluation du potentiel de nouveaux candidats vaccins implique dès lors la caractérisation exhaustive de la réponse immunitaire induite.

La « heparin-binding hemagglutinin (HBHA) » est une protéine de 28-kDa, sécrétée et exprimée à la surface de M. tuberculosis et de M. bovis BCG. Montrant une affinité importante pour les gycoconjugués sulfatés, elle favorise la dissémination hématogène du bacille de Koch.

Nos résultats démontrent que la HBHA stimule l’immunité à médiation cellulaire humaine avec, toutefois, des différences selon que le sujet infecté souffre ou non de tuberculose active. En effet, les cellules mononuclées circulantes, de la majorité des individus infectés mais non-malades, secrètent de l’IFN-? en réponse à la HBHA, alors qu’une minorité de sujets malades produit de faibles quantités d’IFN-? après stimulation in vitro avec l’antigène. Lors de l’infection naturelle par le bacille de Koch, la HBHA devient dès lors une cible pour le système immunitaire, et plus particulièrement au sein des sujets, généralement considérés, comme protégés.

L’analyse de la réponse cellulaire, spécifique à l’adhésine, démontre que les lymphocytes T CD4+, mais également T CD8+, des sujets infectés mais non-malades, produisent de l’IFN-? L’antigène est effectivement présenté aux lymphocytes T grâce aux glycoprotéines du complexe majeur d’histocompatibilité de classe I et de classe II. Le phénotypage des cellules productrices d’IFN-? témoigne également la participation des cellules « natural killer (NK) » dans la réponse immunitaire contre la HBHA. En l’absence des lymphocytes T restreints à l’antigène, les cellules NK se montrent toutefois incapables de secréter de l’IFN-? au contact de la HBHA. Les interactions entre les lymphocytes T, spécifiques à l’antigène, déterminent également la production de cytokines. Alors que la déplétion des cellules T CD8+ diminue légèrement la production d’IFN-? l’absence des lymphocytes T CD4+ abolit toute sécrétion résiduelle d’IFN-? lors de la stimulation avec la HBHA. Par contre, les lymphocytes T CD8+, pré-stimulés avec l’antigène en présence de cellules T CD4+, répondent secondairement à la présentation de la HBHA par des macrophages. Ce résultat suggère une coopération entre ces deux sous-populations cellulaires, afin de produire de l’IFN-? à l’encontre de la HBHA. Grâce à un contact cellulaire, les lymphocytes T CD4+ spécifiques à la HBHA soutiennent effectivement l’activation des cellules T CD8+.

Outre la production de cytokines, la participation des lymphocytes T CD8+ à la lutte contre M. tuberculosis, se traduit également par leurs fonctions cytotoxique et bactéricide. La caractérisation des cellules T CD8+, spécifiques à la HBHA, s’est dès lors poursuivie par l’évaluation de leur potentiel cytolytique. Après expansion clonale, les lymphocytes T CD8+ induisent la mort des macrophages présentant la HBHA. Le mécanisme cytotoxique engage la libération du contenu des granules cytoplasmiques, comme le montre l’augmentation de la synthèse de perforine et de granzyme A, lorsque les cellules T CD8+ sont stimulées avec la HBHA. Privés de ces médiateurs solubles, les lymphocytes T CD8+, spécifiques à la HBHA sont alors incapables de lyser les cellules cibles. En définitive, l’activité microbicide constitue actuellement le meilleur corrélat de protection. La culture de macrophages infectés par M. bovis BCG, en présence de cellules T CD8+ spécifiques à la HBHA, limite partiellement la croissance de la bactérie phagocytée, soulignant le pouvoir anti-mycobactérien de l’immunité cellulaire induite par la HBHA, chez le sujet infecté mais non-malade.

D’autre part, l’analyse biochimique, menée à l’Institut Pasteur de Lille, démontre que la HBHA subit une modification post-traductionnelle, lors de sa synthèse. Il s’agit d’une méthylation des multiples résidus lysine, qui composent son extrémité C-terminale. La comparaison des formes native méthylée et recombinante non-méthylée de la HBHA démontre que la méthylation détermine l’immunogénicité et le pouvoir protecteur de la HBHA. En effet, contrairement à la HBHA native, la forme recombinante stimule faiblement la production d’IFN-? chez les individus infectés mais non-malades, et ne protège pas la souris contre l’infection par le bacille de Koch. La sécrétion d’IFN-? est, par ailleurs, partiellement restaurée lorsque la HBHA est artificiellement méthylée in vitro. Les splénocytes murins se comportent également différemment, selon qu’ils ont été immunisés avec la forme méthylée ou non. Alors que la HBHA recombinante est immunogène chez la souris et chez l’homme, l’immunité cellulaire murine induite demeure impassible face à l’infection des phagocytes par les mycobactéries, ce qui se traduit par l’absence de protection.

En conclusion, la HBHA se compose d’épitopes protecteurs, qui dépendent de la présence des groupements méthyls, associés à son domaine C-terminal. Il s’agit, à notre connaissance, de la première mise en évidence de l’implication de la méthylation dans la réponse d’immunité cellulaire à l’encontre d’une protéine. De plus, l’immunité adaptative spécifique à la HBHA, chez le sujet infecté mais non-malade, se caractérise par les trois principaux corrélats de protection, actuellement décrits chez l’homme. Le potentiel vaccinal de cette adhésine mycobactérienne est donc bien réel.
Doctorat en sciences biomédicales
info:eu-repo/semantics/nonPublished

APA, Harvard, Vancouver, ISO, and other styles
7

Sigola, Lynnette Brenda. "The role of innate immunity in the host response to Mycobacterium bovis." Thesis, London School of Hygiene and Tropical Medicine (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265950.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Lorgat, Faizel. "Proliferative and cytotoxic cellular immune responses in human tuberculosis." Thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/26373.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Beamer, Gillian L. "IMMUNOLOGIC MECHANISMS AND PREDICTORS OF SUSCEPTIBILITY TO MYCOBACTERIUM TUBERCULOSIS." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243993142.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Sfondrini, Lucia. "Enhancement of anti-tumour immunity by transduction with a Mycobacterium tuberculosis gene." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342892.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Tuberculosis immunity"

1

Immunity to mycobactera. New York: Springer-Verlag, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Divangahi, Maziar, ed. The New Paradigm of Immunity to Tuberculosis. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6111-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Shurygin, A. I͡A. Stimuli͡at͡sii͡a protivotuberkuleznogo immuniteta kumysom iz korovʹego i kobylʹego moloka. Rostov-na-Donu: Izd-vo Rostovskogo universiteta, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Fairbairn, Ian Paul. Investigations of a novel mechanism of anti-tuberculous immunity mediated by purinergic (P2X[inferior seven]) receptors. Birmingham: University of Birmingham, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Lurie, Max B. Resistance to Tuberculosis. Harvard University Press, 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

The New Paradigm Of Immunity To Tuberculosis. Springer-Verlag New York Inc., 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Divangahi, Maziar. The New Paradigm of Immunity to Tuberculosis. Springer, 2015.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Savage, Michael. Diseases without Borders: Boosting Your Immunity Against Infectious Diseases from the Flu and Measles to Tuberculosis. Center Street, 2016.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

E, Taylor Christopher, ed. Nutritional abnormalities in infectious diseases: Effects on tuberculosis and AIDS. New York: Haworth Medical Press, 1997.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Academy of Science of South Africa., ed. HIV/AIDS, TB and nutrition: Scientific inquiry into the nutritional influences on human immunity with special reference to HIV infection and active TB in South Africa. Pretoria, South Africa: Academy of Science of South Africa, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Tuberculosis immunity"

1

Harris, James, Sergio De Haro, and Vojo Deretic. "Autophagy and Mycobacterium tuberculosis." In Autophagy in Immunity and Infection, 127–38. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/352760880x.ch6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

van Crevel, Reinout, Tom H. M. Ottenhoff, and Jos W. M. van der Meer. "Innate Immunity to Mycobacterium Tuberculosis." In Tropical Diseases, 241–47. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0059-9_20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Brighenti, Susanna, and Diane J. Ordway. "Regulation of Immunity to Tuberculosis." In Tuberculosis and the Tubercle Bacillus, 73–93. Washington, DC, USA: ASM Press, 2017. http://dx.doi.org/10.1128/9781555819569.ch3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

MacMicking, J. D., and J. D. McKinney. "Macrophage Immunity and Mycobacterium tuberculosis." In Handbook of Experimental Pharmacology, 409–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55742-2_22.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Hanekom, Willem A., and Joel D. Ernst. "Maintenance of Latent Infection, with Correlates of Protective Immunity." In Handbook of Tuberculosis, 279–304. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527611614.ch28.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Wallis, Robert S., and Jerrold J. Ellner. "Immunology of M. tuberculosis and Other Mycobacteria." In Pulmonary Infections and Immunity, 129–48. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-1063-9_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Young, Douglas, and Anne O'Garra. "Mycobacterium tuberculosis and its Ability to Resist Immunity." In Decoding the Genomic Control of Immune Reactions, 169–80. Chichester, UK: John Wiley & Sons, Ltd, 2007. http://dx.doi.org/10.1002/9780470062128.ch14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Raffel, Sidney. "The Mechanism Involved in Acquired Immunity to Tuberculosis." In Ciba Foundation Symposium - Experimental Tuberculosis: Bacillus and Host (with an Addendum on Leprosy), 261–82. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718933.ch20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Ruibal, Paula, Tom H. M. Ottenhoff, and Simone A. Joosten. "Conventional and Unconventional Lymphocytes in Immunity Against Mycobacterium tuberculosis." In Advances in Host-Directed Therapies Against Tuberculosis, 133–68. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56905-1_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Goldberg, Michael F., Neeraj K. Saini, and Steven A. Porcelli. "Evasion of Innate and Adaptive Immunity by Mycobacterium tuberculosis." In Molecular Genetics of Mycobacteria, 747–72. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555818845.ch36.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Tuberculosis immunity"

1

Zhuravlev, Viacheslav, Marina Dyakova, Dilyara Esmedlyaeva, and Tatiana Perova. "Markers of cellular immunity in the diagnosis of tuberculosis pleurisy." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2711.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Matveyeva, Svitlana, Olga Shevchenko, and Olga Pogorelova. "Influence of thyroid function activity on the indexis of immunity in tuberculosis patients." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2714.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Pennington, K., T. Peikert, V. Van Keulen, C. Erskine, and P. Escalante. "Candida-Antigen Immune Reactivity in Subjects with Latent Tuberculosis Infection: A Shared Immunity?" In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6092.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Strawbridge, HD, Y. Lin, J. Rangel-Moreno, S. Ritchea, A. Logar, T. Randall, J. Kolls, and S. Khader. "IL-17 Is Critical for the Generation of Protective Vaccine-Induced Immunity Against Tuberculosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5910.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Widyaningsih, Purnami, Arifin Aji Nugroho, and Dewi Retno Sari Saputro. "Susceptible infected recovered model with vaccination, immunity loss, and relapse to study tuberculosis transmission in Indonesia." In Proceedings of the 17th International Conference on Ion Sources. Author(s), 2018. http://dx.doi.org/10.1063/1.5054525.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Fajardo, Elaine, Rodney Dawson, William N. Rom, and Michael D. Weiden. "Th-1 And Th-2 BAL Cytokine Production Correlates With Sputum Conversion And Cellular Immunity In Pulmonary Tuberculosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3342.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Erra, A., H. Borrell, L. López, and X. Martinez. "AB1284 Preliminary data of vaccination status, post vaccination immunity and latent tuberculosis in patients with chronic inflammatory disease in a rheumatology consultation in st rafael’s hospital in barcelona." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4406.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Divangahi, M., M. Chen, H. Gan, HG Remold, and SM Behar. "Necrotic Death of Infected Macrophages AllowsMycobacterium tuberculosisTo Evade Innate Immune Mechanisms and Delay Initiation of T Cell Immunity." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5750.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Tuberculosis immunity' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography