The innate immune response in human tuberculosis

Lerner, Thomas R.; Borel, Sophie; Gutierrez, Maximiliano G.

doi:10.1111/cmi.12480

Cited by 113 publications

(104 citation statements)

References 83 publications

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“…It is important to bear in mind that MHC-identical MCMs are not necessarily genetically identical outside the MHC, which may explain why our results contrast with the observation that monozygotic twin marmosets infected with the same strains of M. tuberculosis exhibited similar disease courses (36). In addition, the secretion of cytokines and presentation of antigens by macrophages, dendritic cells, or other innate cell types to initiate the adaptive immune response are well established to play a critical role in controlling M. tuberculosis replication and determining overall TB resistance (37)(38)(39). Ultimately, MHCmatched MCMs infected with the same dose and strain of M. tuberculosis may be valuable for defining non-MHC determinants of TB disease.…”

Section: Discussioncontrasting

confidence: 57%

Characterization of T Cells Specific for CFP-10 and ESAT-6 in Mycobacterium tuberculosis-Infected Mauritian Cynomolgus Macaques

et al. 2017

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Nonhuman primates can be used to study host immune responses to Mycobacterium tuberculosis. Mauritian cynomolgus macaques (MCMs) are a unique group of animals that have limited major histocompatibility complex (MHC) genetic diversity, such that MHC-identical animals can be infected with M. tuberculosis. Two MCMs homozygous for the relatively common M1 MHC haplotype were bronchoscopically infected with 41 CFU of the M. tuberculosis Erdman strain. Four other MCMs, which had at least one copy of the M1 MHC haplotype, were infected with a lower dose of 3 CFU M. tuberculosis. All animals mounted similar T-cell responses to CFP-10 and ESAT-6. Two epitopes in CFP-10 were characterized, and the MHC class II alleles restricting them were determined. A third epitope in CFP-10 was identified but exhibited promiscuous restriction. The CFP-10 and ESAT-6 antigenic regions targeted by T cells in MCMs were comparable to those seen in cases of human M. tuberculosis infection. Our data lay the foundation for generating tetrameric molecules to study epitope-specific CD4 T cells in M. tuberculosis-infected MCMs, which may guide future testing of tuberculosis vaccines in nonhuman primates.

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Section: Discussioncontrasting

confidence: 57%

Characterization of T Cells Specific for CFP-10 and ESAT-6 in Mycobacterium tuberculosis-Infected Mauritian Cynomolgus Macaques

et al. 2017

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“…These responses are an integral component of host defence and bacterial containment 34,43,44,61 , and they are intimately linked with granuloma outcome 37,62–64 . The particular immune cells involved in TB immunity 34,65–67 , and their localization and kinetics 32,41,61,68 , have been extensively reviewed in the past few years.…”

Section: Granuloma Heterogeneitymentioning

confidence: 99%

Heterogeneity in tuberculosis

2017

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Infection with Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), results in a range of clinical presentations in humans. Most infections manifest as a clinically asymptomatic, contained state that is termed latent TB infection (LTBI); a smaller subset of infected individuals present with symptomatic, active TB. Within these two seemingly binary states, there is a spectrum of host outcomes that have varying symptoms, microbiologies, immune responses and pathologies. Recently, it has become apparent that there is diversity of infection even within a single individual. A good understanding of the heterogeneity that is intrinsic to TB — at both the population level and the individual level — is crucial to inform the development of intervention strategies that account for and target the unique, complex and independent nature of the local host–pathogen interactions that occur in this infection. In this Review, we draw on model systems and human data to discuss multiple facets of TB biology and their relationship to the overall heterogeneity observed in the human disease.

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“…In addition, macrophages generate nitric oxide and reactive oxygen species, T-cells, and natural killer (NK) cells [36, 37]. In the context of obesity-related diabetes, increased pro-inflammatory cytokines, reactive oxygen species, and nitric oxide cause insulin resistance through a cascade of inflammation pathways leading to hyperglycemia [38–40].…”

Section: Section 2: Pathophysiology Of Tb Disease and Stress Hyperglymentioning

confidence: 99%

Stress Hyperglycemia in Patients with Tuberculosis Disease: Epidemiology and Clinical Implications

et al. 2018

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Among patients with TB disease, the development of stress hyperglycemia may influence the clinical manifestation and treatment response of some patients and can complicate diabetes diagnosis. Research is needed to elucidate the relationship between TB disease and stress hyperglycemia and determine the extent to which stress hyperglycemia impacts TB treatment response. Currently, there is insufficient data to support clinical recommendations for glucose control among patients with TB disease, representing a major barrier for efforts to improve treatment outcomes for patients with TB and diabetes.

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The innate immune response in human tuberculosis

Cited by 113 publications

References 83 publications

Characterization of T Cells Specific for CFP-10 and ESAT-6 in Mycobacterium tuberculosis-Infected Mauritian Cynomolgus Macaques

Characterization of T Cells Specific for CFP-10 and ESAT-6 in Mycobacterium tuberculosis-Infected Mauritian Cynomolgus Macaques

Heterogeneity in tuberculosis

Stress Hyperglycemia in Patients with Tuberculosis Disease: Epidemiology and Clinical Implications

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