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Journal articles on the topic 'Tuberculosis immunity'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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11

York, Ashley. "M. tuberculosis stifles trained immunity." Nature Reviews Microbiology 19, no. 1 (November 5, 2020): 2. http://dx.doi.org/10.1038/s41579-020-00479-3.

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12

Martinez, Nuria, and Hardy Kornfeld. "Diabetes and immunity to tuberculosis." European Journal of Immunology 44, no. 3 (February 16, 2014): 617–26. http://dx.doi.org/10.1002/eji.201344301.

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13

Langan, Emma I. "The Brontës and Tuberculosis Immunity." Brontë Studies 46, no. 2 (March 26, 2021): 210–22. http://dx.doi.org/10.1080/14748932.2021.1875635.

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14

Meraviglia, Serena, Sary El Daker, Francesco Dieli, Federico Martini, and Angelo Martino. "γδT Cells Cross-Link Innate and Adaptive Immunity inMycobacterium tuberculosisInfection." Clinical and Developmental Immunology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/587315.

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Protective immunity against mycobacterial infections such asMycobacterium tuberculosisis mediated by interactions between specific T cells and activated antigen presenting cells. To date, many aspects of mycobacterial immunity have shown that innate cells could be the key elements that substantially may influence the subsequent adaptive host response. During the early phases of infection, innate lymphocyte subsets play a pivotal role in this context. Here we summarize the findings of recent investigations onγδT lymphocytes and their role in tuberculosis immunity.

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15

Madan-Lala, Ranjna, Katia Vitorello Peixoto, Fabio Re, and Jyothi Rengarajan. "Mycobacterium tuberculosis Hip1 Dampens Macrophage Proinflammatory Responses by Limiting Toll-Like Receptor 2 Activation." Infection and Immunity 79, no. 12 (September 26, 2011): 4828–38. http://dx.doi.org/10.1128/iai.05574-11.

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ABSTRACTMycobacterium tuberculosisis a highly successful human pathogen that evades host innate immunity by interfering with macrophage functions. In addition to avoiding macrophage microbicidal activities,M. tuberculosistriggers secretion of proinflammatory cytokines and chemokines in macrophages. The levels of proinflammatory cytokines induced by clinicalM. tuberculosisisolates are thought to play an important role in determining tuberculosis disease progression and severity, but the mechanisms by whichM. tuberculosismodulates the magnitude of inflammatory responses remain unclear. Here we show thatM. tuberculosisrestricts robust macrophage activation and dampens proinflammatory responses through the cell envelope-associated serine hydrolase Hip1 (hydrolaseimportant forpathogenesis1). By transcriptionally profiling macrophages infected with either wild-type orhip1mutant bacteria, we found that thehip1mutant induced earlier and significantly higher levels of several proinflammatory cytokines and chemokines. We show that increased activation of Toll-like receptor 2 (TLR2)- and MyD88-dependent signaling pathways mediates the enhanced cytokine secretion induced by thehip1mutant. Thus, Hip1 restricts the onset and magnitude of proinflammatory cytokines by limiting TLR2-dependent activation. We also show that Hip1 dampens TLR2-independent activation of the inflammasome and limits secretion of interleukin-18 (IL-18). Dampening of TLR2 signaling does not require viableM. tuberculosisor phagocytosis but does require Hip1 catalytic activity. We propose thatM. tuberculosisrestricts proinflammatory responses by masking cell surface interactions between TLR2 agonists onM. tuberculosisand TLR2 on macrophages. This strategy may allowM. tuberculosisto evade early detection by host immunity, delay the onset of adaptive immune responses, and accelerate disease progression.

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16

Zlata, Hajric Zidan, Pasic Amela, and Selimovic Selma. "Silent Brain Tuberculomas with Acute Miliary Tuberculosis in 13-Year Old Girl - Case Report." International Journal of Health Sciences and Research 11, no. 6 (June 10, 2021): 145–47. http://dx.doi.org/10.52403/ijhsr.20210621.

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We describe iron deficiency and silent intracranial tuberculomas with pulmonary miliary tuberculosis in 13-year old girl which can be rare seen, particularly in immunocompetent children. She presented as respiratory infection with lack of menstrual bleeding. She didn’t receive BCG vaccination. Chest roentgenogram showed miliary pattern while MRI of brain revealed parenchymal tuberculomas. Empirical 4 antitubercular drug treatments were initiated. Control showed a decrease in size and number of brain tuberculomas. Silent brain tuberculomas with miliary tuberculosis could be rare seen, particularly in immunocompetent children. It remains an open question whether the irregular menstrual bleeding and iron deficiency was associated with the drop of her immunity and increased risk for military tuberculosis. Key words: BCG vaccination, irregular menstrual bleeding, MRI of endocranium.

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17

Korb, Vanessa, Anil Chuturgoon, and Devapregasan Moodley. "Mycobacterium tuberculosis: Manipulator of Protective Immunity." International Journal of Molecular Sciences 17, no. 3 (February 25, 2016): 131. http://dx.doi.org/10.3390/ijms17030131.

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18

Martínez-Romero, Aurora, José Luis Ortega-Sánchez, Norma Urtiz-Estrada, Esperanza Yasmín Calleros-Rincón, Rebeca Pérez-Morales, and José de Jesús Alba-Romero. "Immunity towards tuberculosis infection: A review." African Journal of Microbiology Research 9, no. 37 (September 16, 2015): 2013–22. http://dx.doi.org/10.5897/ajmr2015.7033.

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19

Khader, Shabaana A., Maziar Divangahi, Willem Hanekom, Philip C. Hill, Markus Maeurer, Karen W. Makar, Katrin D. Mayer-Barber, et al. "Targeting innate immunity for tuberculosis vaccination." Journal of Clinical Investigation 129, no. 9 (September 3, 2019): 3482–91. http://dx.doi.org/10.1172/jci128877.

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20

Rozov, S. M., N. A. Popova, and E. V. Deineko. "Immunity against Mycobacterium tuberculosis: Defense strategies." Biology Bulletin Reviews 6, no. 6 (November 2016): 483–96. http://dx.doi.org/10.1134/s2079086416060062.

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21

Sehgal, V. N., P. Ahuju, and V. K. Sharma. "Cell-mediated immunity in cutaneous tuberculosis." British Journal of Dermatology 118, no. 5 (May 1988): 730. http://dx.doi.org/10.1111/j.1365-2133.1988.tb02582.x.

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22

Blanc, Landry, Martine Gilleron, Jacques Prandi, Ok-ryul Song, Mi-Seon Jang, Brigitte Gicquel, Daniel Drocourt, et al. "Mycobacterium tuberculosisinhibits human innate immune responses via the production of TLR2 antagonist glycolipids." Proceedings of the National Academy of Sciences 114, no. 42 (October 2, 2017): 11205–10. http://dx.doi.org/10.1073/pnas.1707840114.

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Mycobacterium tuberculosisis a major human pathogen that is able to survive inside host cells and resist immune clearance. Most particularly, it inhibits several arms of the innate immune response, including phagosome maturation or cytokine production. To better understand the molecular mechanisms by whichM. tuberculosiscircumvents host immune defenses, we used a transposon mutant library generated in a virulent clinical isolate ofM. tuberculosisof the W/Beijing family to infect human macrophages, utilizing a cell line derivative of THP-1 cells expressing a reporter system for activation of the transcription factor NF-κB, a key regulator of innate immunity. We identified severalM. tuberculosismutants inducing a NF-κB activation stronger than that of the wild-type strain. One of these mutants was found to be deficient for the synthesis of cell envelope glycolipids, namely sulfoglycolipids, suggesting that the latter can interfere with innate immune responses. Using natural and synthetic molecular variants, we determined that sulfoglycolipids inhibit NF-κB activation and subsequent cytokine production or costimulatory molecule expression by acting as competitive antagonists of Toll-like receptor 2, thereby inhibiting the recognition ofM. tuberculosisby this receptor. Our study reveals that producing glycolipid antagonists of pattern recognition receptors is a strategy used byM. tuberculosisto undermine innate immune defense. Sulfoglycolipids are major and specific lipids ofM. tuberculosis, considered for decades as virulence factors of the bacilli. Our study uncovers a mechanism by which they may contribute toM. tuberculosisvirulence.

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23

Glatman-Freedman, Aharona, and Arturo Casadevall. "Serum Therapy for Tuberculosis Revisited: Reappraisal of the Role of Antibody-Mediated Immunity againstMycobacterium tuberculosis." Clinical Microbiology Reviews 11, no. 3 (July 1, 1998): 514–32. http://dx.doi.org/10.1128/cmr.11.3.514.

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SUMMARY Fifty years after the introduction of the first effective antimicrobial agents against Mycobacterium tuberculosis, this pathogen continues to be a tremendous public health problem. The rise in the number of resistant strains and the difficulties involved in the therapy of tuberculosis in immunocompromised AIDS patients have renewed the interest in the development of effective vaccines. To evaluate whether a potential vaccine against tuberculosis could prevent infection by eliciting a protective antibody response, we reviewed the history of antibody-mediated immunity against tuberculosis. Review of the literature of the past 100 years demonstrates that there is sufficient evidence to conclude that antibody-mediated immunity can modify the course of infection in certain situations. Based on our findings and on what is known in other systems, we propose that the role of antibody-mediated immunity to M. tuberculosis be reexamined, using advanced technology.

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24

Lesnic, Evelina, Serghei Ghinda, and Carmen Monica Pop. "The impact of immune disturbances on the failure of antituberculosis treatment." Medicine and Pharmacy Reports 89, no. 4 (October 28, 2016): 493–98. http://dx.doi.org/10.15386/cjmed-609.

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Background and aim. Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis complex, with an evolution and treatment outcome determined by the interaction between the mycobacterial and human genotypes. Various deficiencies of innate immune response starting from the first encounter of M. tuberculosis with lung cells endanger host infection control due to decreased triggering of cellular immune resistance and disturbed humoral immunity. Disturbed cell mediated immunity, known as the basic immune response in tuberculous infection, contributes to the deficient generation of central necrosis granuloma, consequently being responsible for severe clinical aspects and low final outcome. The tuberculosis patient’s immune assessment is important before treatment initiation, for establishing the risk reduction measures and increasing success rate.Material and methods. The immune study was conducted on 54 new pulmonary tuberculosis cases with treatment failure, 34 new pulmonary tuberculosis cases that successfully ended the treatment and 50 healthy group individuals. Immune assays performed were: blastic transformation of lymphocytes induced by different antigens, quantitatitve assessment of cellular immunity through CD4+ T cell and CD8+ T cell phenotyping, humoral immunity - through immunoglobulin isotyping, innate resistance – through phagocyte activity of neutrophils, the titter of anti-tuberculosis antibodies and the serum level of circulating immune complexes. Investigations were performed at the onset the treatment and at the end of intensive phase of the standard anti-tuberculosis treatment.Results. Immune disturbances evidenced in patients with treatment failure were: important deficiencies of cellular immunity, hyperactivity of humoral immunity and deficiencies of innate immunity. High predictive value for treatment failure showed the indices: deficiency of T lymphocytes count (OR=62.5) and T helper count (OR=12.5), high level of circulating immune complexes (OR=9.801), deficiency of innate resistance (decreased phagocytating index OR=2.875).Conclusions. For increasing the treatment success rate, the study of immune disturbances must be performed before of antituberculosis treatment initiation , especially of cellular immunity for the early start of immune adaptive treatment.

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25

Lapshtaeva, A. V., E. A. Zhivechkova, I. V. Sychev, I. V. Evsegneeva, and V. V. Novikov. "Innate immune receptors in development of Mycobacterium tuberculosis infection." Russian Journal of Infection and Immunity 10, no. 1 (April 7, 2020): 35–48. http://dx.doi.org/10.15789/2220-7619-roi-1169.

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According to the World Health Organization, over 10 million new tuberculosis cases are reported annually worldwide. According to the 2017 Federal State Statistics Service Report, incidence rate for active TB infection in the Russian Federation was 109.8 cases per 100,000 population, of which 41.3% accounted for chronic disease form. Regardless of climatic conditions, high prevalence of TB infection, is not only due to high Mycobacterium tuberculosis viability, but also its ability for long persistence in human body and reactivation after an unlimited period of dormancy. The outcome of infection is largely determined by host immunoreactivity and its ability to develop protective immune response. In addition, status of immune system also underlies tuberculosis course after the onset: either as a localized form, or as a form with extensive damage to the lungs and even other organs observed in generalized infection. In recent decades, a great attention was paid to examining mechanisms of adaptive cell immunity played in pathogenesis of TB infection. No doubt, adaptive immunity is a powerful defense system providing a targeted specific immune response, but now it is becoming clear that it represents solely an effector arm of innate immunity. Innate immunity is a phylogenetically more ancient, inherited system largely aimed at ensuring rapid pathogen elimination and preventing development of infection at early stages when adaptive immunity ongoing antigen-specific maturation. Mechanisms of innate immunity mediated by cells, diverse receptors, molecules and their complexes, found on various cells. Activation of innate immunity begins with recognition of conserved molecular groups present in various pathogens called pathogen-associated molecular patterns (PAMPs), which are sensed by pathogen recognition receptors (PRRs). Here, we review current data on the role of innate receptors in recognizing M. tuberculosis-derived PAMPs, production of immunoregulatory cytokines and activation of signaling pathways playing a crucial role in the regulation of necroptosis, apoptosis and autophagy of infected macrophages. Significance of innate mucosal factors in implementing immune response to M. tuberculosis is discussed. In particular, Toll-like receptors, scavenger-receptors, mannose receptor, DC-SIGN etc. were described to participate in development of M. tuberculosis immunity. The data on single nucleotide polymorphic variants for innate genes are shown, which predispose to developing tuberculosis and affecting its course.

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26

Niki, Mamiko, Takashi Yoshiyama, Yuji Miyamoto, Masao Okumura, Makoto Niki, Ken-ichi Oinuma, Yukihiro Kaneko, et al. "Longitudinal Evaluation of Humoral Immunity and Bacterial and Clinical Parameters Reveals That Antigen-Specific Antibodies Suppress Inflammatory Responses in Active Tuberculosis Patients." Journal of Immunology Research 2018 (July 4, 2018): 1–11. http://dx.doi.org/10.1155/2018/4928757.

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A novel tuberculosis vaccine to replace BCG has long been desired. However, recent vaccine trials focused on cell-mediated immunity have failed to produce promising results. It is worth noting that most commercially available successful vaccines rely on humoral immunity. To establish a basic understanding of humoral immunity against tuberculosis, we analyzed and evaluated longitudinal levels and avidity of immunoglobulin to various tuberculosis antigens compared with bacterial and clinical parameters during treatment. We found that levels of IgG antibodies against HrpA and HBHA prior to treatment exhibited a positive correlation with bacterial burden. Analysis of changes in CRP during treatment revealed an association with high levels of specific IgG and IgA antibodies against mycobacterial antigens. Levels of CRP prior to treatment were negatively associated with IgG avidity to CFP-10 and MDP1 and IgA avidity to HrpA, while IgA avidity to MDP1 and Acr exhibited a negative correlation with CRP levels after 60 days of treatment. These results may provide insight for the development of a novel tuberculosis (TB) vaccine candidate to induce protective humoral immunity against tuberculosis.

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27

Vogelzang, Alexis, Laura Lozza, Stephen T. Reece, Carolina Perdomo, Ulrike Zedler, Karin Hahnke, Dagmar Oberbeck-Mueller, Anca Dorhoi, and Stefan H. E. Kaufmann. "Neonatal Fc Receptor Regulation of Lung Immunoglobulin and CD103+Dendritic Cells Confers Transient Susceptibility to Tuberculosis." Infection and Immunity 84, no. 10 (August 1, 2016): 2914–21. http://dx.doi.org/10.1128/iai.00533-16.

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The neonatal Fc receptor (FcRn) extends the systemic half-life of IgG antibodies by chaperoning bound Fc away from lysosomal degradation inside stromal and hematopoietic cells. FcRn also transports IgG across mucosal barriers into the lumen, and yet little is known about how FcRn modulates immunity in the lung during homeostasis or infection. We infected wild-type (WT) and FcRn-deficient (fcgrt−/−) mice withPseudomonas aeruginosaorMycobacterium tuberculosisto investigate whether recycling and transport of IgG via FcRn influences innate and adaptive immunity in the lung in response to bacterial infection. We found that FcRn expression maintains homeostatic IgG levels in lung and leads to preferential secretion of low-affinity IgG ligands into the lumen.Fcgrt−/−animals exhibited no evidence of developmental impairment of innate immunity in the lung and were able to efficiently recruit neutrophils in a model of acute bacterial pneumonia. Although local humoral immunity in lung increased independently of the presence of FcRn during tuberculosis, there was nonetheless a strong impact of FcRn deficiency on local adaptive immunity. We show that the quantity and quality of IgG in airways, as well as the abundance of dendritic cells in the lung, are maintained by FcRn. FcRn ablation transiently enhanced local T cell immunity and neutrophil recruitment during tuberculosis, leading to a lower bacterial burden in lung. This novel understanding of tissue-specific modulation of mucosal IgG isotypes in the lung by FcRn sheds light on the role of mucosal IgG in immune responses in the lung during homeostasis and bacterial disease.

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28

Matvyeye, S. L., and O. S. Shevchenko. "Immunity indicators in tuberculosis patients with diabetes mellitus and autoimmune thyroiditis." Tuberculosis, Lung Diseases, HIV Infection, no. 2 (June 29, 2021): 26–30. http://dx.doi.org/10.30978/tb2021-2-26.

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Objective — to study the parameters of immunity in tuberculosis with diabetes mellitus and with subclinical hypothyroidism against the background of autoimmune thyroiditis. Materials and methods. 60 patients with pulmonary tuberculosis and diabetes mellitus were under observation. In 30 patients with destructive tuberculosis and diabetes mellitus against the background of autoimmune thyroiditis with subclinical hypothyroidism, the parameters of humoral and cellular immunity were studied. The control group consisted of 30 patients with destructive tuberculosis and diabetes mellitus with intact structure and function of the thyroid gland. In patients of both groups, we assessed the state of T- and B-systems of immunity, natural killers. Results and discussion. The phenotyping of lymphocytes was carried out and the relative content of T-cells was determined: CD3+, T-helpers (CD4+), cytotoxic T-cells, B-lymphocytes (CD19+) and natural killer cells (CD16+). Using the enzyme immunoassay, the cytokine profile was determined: the levels of tumor necrosis factor-α, interferon-γ, interleukin-2, -6 and -4. It has been established that in patients with diabetes mellitus, both cellular and humoral immunity are suppressed. But a significantly more significant suppression of immunity was diagnosed in patients with tuberculosis against the background of diabetes mellitus and autoimmune thyroiditis with subclinical hypothyroidism. Conclusions. According to the authors, it is the deficiency of thyroid hormones that is the negative effect of a more significant suppression of immunity in patients autoimmune thyroiditis with subclinical hypothyroidism.

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29

Magrone, Thea, and Emilio Jirillo. "Immunity to Tuberculosis and Novel Therapeutic Strategies." Clinical Immunology, Endocrine & Metabolic Drugs 1, no. 1 (July 20, 2014): 46–60. http://dx.doi.org/10.2174/221270700101140721001419.

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30

da Fonseca, D. P. A. J., A. F. M. Verheul, and H. Snippe. "Induction of cellular immunity against Mycobacterium tuberculosis." Immunology Letters 56 (May 1997): 446. http://dx.doi.org/10.1016/s0165-2478(97)86813-7.

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31

Korbel, Daniel S., Bianca E. Schneider, and Ulrich E. Schaible. "Innate immunity in tuberculosis: myths and truth." Microbes and Infection 10, no. 9 (July 2008): 995–1004. http://dx.doi.org/10.1016/j.micinf.2008.07.039.

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32

BIRKHAUG, KONRAD. "Allergy and immunity (iathergy) in experimental tuberculosis." Acta Medica Scandinavica 110, no. 2-3 (April 24, 2009): 201–29. http://dx.doi.org/10.1111/j.0954-6820.1942.tb13077.x.

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33

BIRKHAUG, KONRAD, and EINAR BERLE. "Allergy and immunity (iathergy) in experimental tuberculosis." Acta Medica Scandinavica 121, no. 2-3 (April 24, 2009): 115–31. http://dx.doi.org/10.1111/j.0954-6820.1945.tb06872.x.

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34

Stenger, Steffen, and Robert L. Modlin. "T cell mediated immunity to Mycobacterium tuberculosis." Current Opinion in Microbiology 2, no. 1 (February 1999): 89–93. http://dx.doi.org/10.1016/s1369-5274(99)80015-0.

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35

Andrade-Arzabe, Ronald, Irma V. Machado, Beatriz Fernandez, Isaac Blanca, Romelia Ramirez, and Nicolas E. Bianco. "Cellular Immunity in Current Active Pulmonary Tuberculosis." American Review of Respiratory Disease 143, no. 3 (March 1991): 496–500. http://dx.doi.org/10.1164/ajrccm/143.3.496.

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36

Mahla, Ranjeet S. "KLRG1 Signaling Is Contextual to Tuberculosis Immunity." Journal of Infectious Diseases 218, no. 8 (May 28, 2018): 1348. http://dx.doi.org/10.1093/infdis/jiy313.

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37

Shah, Javeed A., Cecilia S. Lindestam Arlehamn, David J. Horne, Alessandro Sette, and Thomas R. Hawn. "Nontuberculous Mycobacteria and Heterologous Immunity to Tuberculosis." Journal of Infectious Diseases 220, no. 7 (June 4, 2019): 1091–98. http://dx.doi.org/10.1093/infdis/jiz285.

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AbstractDevelopment of an improved tuberculosis (TB) vaccine is a high worldwide public health priority. Bacillus Calmette-Guerin (BCG), the only licensed TB vaccine, provides variable efficacy against adult pulmonary TB, but why this protection varies is unclear. Humans are regularly exposed to non-tuberculous mycobacteria (NTM) that live in soil and water reservoirs and vary in different geographic regions around the world. Immunologic cross-reactivity may explain disparate outcomes of BCG vaccination and susceptibility to TB disease. Evidence supporting this hypothesis is increasing but challenging to obtain due to a lack of reliable research tools. In this review, we describe the progress and bottlenecks in research on NTM epidemiology, immunology and heterologous immunity to Mtb. With ongoing efforts to develop new vaccines for TB, understanding the effect of NTM on vaccine efficacy may be a critical determinant of success.

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BOTHAMLEY, G. "Does immunity to tuberculosis contribute to pathogenesis?" Journal of the American College of Cardiology 4, no. 3 (March 1996): 95. http://dx.doi.org/10.1016/s0735-1097(96)90275-2.

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Orme, Ian M., and Andrea M. Cooper. "Cytokine/chemokine cascades in immunity to tuberculosis." Immunology Today 20, no. 7 (July 1999): 307–12. http://dx.doi.org/10.1016/s0167-5699(98)01438-8.

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da Fonseca, D. "Induction of cellular immunity against Mycobacterium tuberculosis." Immunology Letters 56, no. 1-3 (May 1997): 446. http://dx.doi.org/10.1016/s0165-2478(97)88653-1.

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Pan, Hui, Bo-Shiun Yan, Mauricio Rojas, Yuriy V. Shebzukhov, Hongwei Zhou, Lester Kobzik, Darren E. Higgins, Mark J. Daly, Barry R. Bloom, and Igor Kramnik. "Ipr1 gene mediates innate immunity to tuberculosis." Nature 434, no. 7034 (April 2005): 767–72. http://dx.doi.org/10.1038/nature03419.

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Waters, W. Ray, Mitchell V. Palmer, Tyler C. Thacker, William C. Davis, Srinand Sreevatsan, Paul Coussens, Kieran G. Meade, Jayne C. Hope, and D. Mark Estes. "Tuberculosis Immunity: Opportunities from Studies with Cattle." Clinical and Developmental Immunology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/768542.

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Mycobacterium tuberculosisandM. bovisshare >99% genetic identity and induce similar host responses and disease profiles upon infection. There is a rich history of codiscovery in the development of control measures applicable to both human and bovine tuberculosis (TB) including skin-testing procedures,M. bovisBCG vaccination, and interferon-γ release assays. The calf TB infection model offers several opportunities to further our understanding of TB immunopathogenesis. Recent observations include correlation of central memory immune responses with TB vaccine efficacy, association of SIRPα+cells in ESAT-6:CFP10-elicited multinucleate giant cell formation, early γδ T cell responses to TB, antimycobacterial activity of memory CD4+T cells via granulysin production, association of specific antibody with antigen burden, and suppression of innate immune gene expression in infected animals. Partnerships teaming researchers with veterinary and medical perspectives will continue to provide mutual benefit to TB research in man and animals.

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Winslow, Gary M., Andrea Cooper, William Reiley, Madhumouli Chatterjee, and David L. Woodland. "Early T-cell responses in tuberculosis immunity." Immunological Reviews 225, no. 1 (October 2008): 284–99. http://dx.doi.org/10.1111/j.1600-065x.2008.00693.x.

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Parlane, Natalie A., and Bryce M. Buddle. "Immunity and Vaccination against Tuberculosis in Cattle." Current Clinical Microbiology Reports 2, no. 1 (January 22, 2015): 44–53. http://dx.doi.org/10.1007/s40588-014-0009-4.

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Swaim, Laura E., Lynn E. Connolly, Hannah E. Volkman, Olivier Humbert, Donald E. Born, and Lalita Ramakrishnan. "Mycobacterium marinum Infection of Adult Zebrafish Causes Caseating Granulomatous Tuberculosis and Is Moderated by Adaptive Immunity." Infection and Immunity 74, no. 11 (November 2006): 6108–17. http://dx.doi.org/10.1128/iai.00887-06.

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ABSTRACT The zebrafish, a genetically tractable model vertebrate, is naturally susceptible to tuberculosis caused by Mycobacterium marinum, a close genetic relative of the causative agent of human tuberculosis, Mycobacterium tuberculosis. We previously developed a zebrafish embryo-M. marinum infection model to study host-pathogen interactions in the context of innate immunity. Here, we have constructed a flowthrough fish facility for the large-scale longitudinal study of M. marinum-induced tuberculosis in adult zebrafish where both innate and adaptive immunity are operant. We find that zebrafish are exquisitely susceptible to M. marinum strain M. Intraperitoneal injection of five organisms produces persistent granulomatous tuberculosis, while the injection of ∼9,000 organisms leads to acute, fulminant disease. Bacterial burden, extent of disease, pathology, and host mortality progress in a time- and dose-dependent fashion. Zebrafish tuberculous granulomas undergo caseous necrosis, similar to human tuberculous granulomas. In contrast to mammalian tuberculous granulomas, zebrafish lesions contain few lymphocytes, calling into question the role of adaptive immunity in fish tuberculosis. However, like rag1 mutant mice infected with M. tuberculosis, we find that rag1 mutant zebrafish are hypersusceptible to M. marinum infection, demonstrating that the control of fish tuberculosis is dependent on adaptive immunity. We confirm the previous finding that M. marinum ΔRD1 mutants are attenuated in adult zebrafish and extend this finding to show that ΔRD1 predominantly produces nonnecrotizing, loose macrophage aggregates. This observation suggests that the macrophage aggregation defect associated with ΔRD1 attenuation in zebrafish embryos is ongoing during adult infection.

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Johnson, Erin E., Andreas Sandgren, Bobby J. Cherayil, Megan Murray, and Marianne Wessling-Resnick. "Role of Ferroportin in Macrophage-Mediated Immunity." Infection and Immunity 78, no. 12 (September 13, 2010): 5099–106. http://dx.doi.org/10.1128/iai.00498-10.

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ABSTRACT Perturbations in iron metabolism have been shown to dramatically impact host response to infection. The most common inherited iron overload disorder results from defects in the HFE gene product, a major histocompatibility complex class I-like protein that interacts with transferrin receptors. HFE-associated hemochromatosis is characterized by abnormally high levels of the iron efflux protein ferroportin. In this study, J774 murine macrophages overexpressing ferroportin were used to investigate the influence of iron metabolism on the release of nitric oxide (NO) in response to infection. Overexpression of ferroportin significantly impaired intracellular Mycobacterium tuberculosis growth during early stages of infection. When challenged with lipopolysaccharide (LPS) or M. tuberculosis infection, control macrophages increased NO synthesis, but macrophages overexpressing ferroportin had significantly impaired NO production in response to LPS or M. tuberculosis. Increased NO synthesis in control cells was accompanied by increased iNOS mRNA and protein, while upregulation of iNOS protein was markedly reduced when J744 cells overexpressing ferroportin were challenged with LPS or M. tuberculosis, thus limiting the bactericidal activity of these macrophages. The proinflammatory cytokine gamma interferon reversed the inhibitory effect of ferroportin overexpression on NO production. These results suggest a novel role for ferroportin in attenuating macrophage-mediated immune responses.

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You, Jiacong. "Research progress on immune response of B lymphocytes and anti-Mycobacterium tuberculosis infection." Infection International 5, no. 1 (March 1, 2016): 1–4. http://dx.doi.org/10.1515/ii-2017-0120.

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Abstract Multiple studies elucidated the importance of cellular immune mechanisms for protection against Mycobacterium tuberculosis. However, recent studies showed that B lymphocytes play a role that is underestimated through various interactions with cellular immune response, forming an important aspect of host defense against M. tuberculosis bacteria. Therefore, the author hereby proposes a progressive perspective for immunology of tuberculosis, i.e., cellular immunity and humoral immunity are not necessarily mutually exclusive. The present study summarizes recent studies that support the important role of B lymphocytes in terms of M. tuberculosis infection.

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Rao Muvva, Jagadeeswara, Sultan Ahmed, Rokeya Sultana Rekha, Sadaf Kalsum, Ramona Groenheit, Thomas Schön, Birgitta Agerberth, Peter Bergman, and Susanna Brighenti. "Immunomodulatory Agents Combat Multidrug-Resistant Tuberculosis by Improving Antimicrobial Immunity." Journal of Infectious Diseases 224, no. 2 (February 19, 2021): 332–44. http://dx.doi.org/10.1093/infdis/jiab100.

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Abstract Background Multidrug-resistant (MDR) tuberculosis has low treatment success rates, and new treatment strategies are needed. We explored whether treatment with active vitamin D3 (vitD) and phenylbutyrate (PBA) could improve conventional chemotherapy by enhancing immune-mediated eradication of Mycobacterium tuberculosis. Methods A clinically relevant model was used consisting of human macrophages infected with M. tuberculosis isolates (n = 15) with different antibiotic resistance profiles. The antimicrobial effect of vitD+PBA, was tested together with rifampicin or isoniazid. Methods included colony-forming units (intracellular bacterial growth), messenger RNA expression analyses (LL-37, β-defensin, nitric oxide synthase, and dual oxidase 2), RNA interference (LL-37-silencing in primary macrophages), and Western blot analysis and confocal microscopy (LL-37 and LC3 protein expression). Results VitD+PBA inhibited growth of clinical MDR tuberculosis strains in human macrophages and strengthened intracellular growth inhibition of rifampicin and isoniazid via induction of the antimicrobial peptide LL-37 and LC3-dependent autophagy. Gene silencing of LL-37 expression enhanced MDR tuberculosis growth in vitD+PBA–treated macrophages. The combination of vitD+PBA and isoniazid were as effective in reducing intracellular MDR tuberculosis growth as a >125-fold higher dose of isoniazid alone, suggesting potent additive effects of vitD+PBA with isoniazid. Conclusions Immunomodulatory agents that trigger multiple immune pathways can strengthen standard MDR tuberculosis treatment and contribute to next-generation individualized treatment options for patients with difficult-to-treat pulmonary tuberculosis.

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Behar, Samuel M., Stephen M. Carpenter, Matthew G. Booty, Daniel L. Barber, and Pushpa Jayaraman. "Orchestration of pulmonary T cell immunity during Mycobacterium tuberculosis infection: Immunity interruptus." Seminars in Immunology 26, no. 6 (December 2014): 559–77. http://dx.doi.org/10.1016/j.smim.2014.09.003.

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Fairbairn, I. P. "Macrophage apoptosis in host immunity to mycobacterial infections." Biochemical Society Transactions 32, no. 3 (June 1, 2004): 496–98. http://dx.doi.org/10.1042/bst0320496.

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Macrophage apoptosis occurs within the granuloma, which is essential for successful immunity to tuberculosis. In vitro macrophage apoptosis is associated with the killing of intracellular Mycobacterium tuberculosis. A greater understanding of these observations will lead to new immunotherapies and improved vaccine design. The relevant apoptotic stimuli, the anti-mycobacterial mechanisms that they stimulate and their physiological relevance are reviewed in this paper.

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