Activating KIRs alter susceptibility to pulmonary tuberculosis in a South African population

Salie, Muneeb; Daya, Michelle; Möller, Marlo; Hoal, Eileen G.

doi:10.1016/j.tube.2015.09.003

Cited by 20 publications

(14 citation statements)

References 24 publications

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“…The results shown that stimulatory genes such as 2DS1, 2DS3 , and 3DS1 associated with resistance to pulmonary tuberculosis ( 122 ). Similar protective association was observed in stimulatory 3DS1 gene in South African colored population ( 123 ). In Lur population of Iran investigated KIR as well as KIR-HLA combinations to TB susceptibility.…”

Section: Genetic Variants and Tb Associationsupporting

confidence: 80%

Influence of Genetic Polymorphism Towards Pulmonary Tuberculosis Susceptibility

2018

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Tuberculosis (TB) is still remains the major threat for human health worldwide. Several case-control, candidate-gene, family studies and genome-wide association studies (GWAS) suggested the association of host genetic factors to TB susceptibility or resistance in various ethnic populations. Moreover, these factors modulate the host immune responses to tuberculosis. Studies have reported genetic markers to predict TB development in human leukocyte antigen (HLA) and non-HLA genes like killer immunoglobulin-like receptor (KIR), toll-like receptors (TLRs), cytokine/chemokines and their receptors, vitamin D receptor (VDR) and SLC11A1 etc. Highly polymorphic HLA loci may influence antigen presentation specificities by modifying peptide binding motifs. The recent meta-analysis studies revealed the association of several HLA alleles in particular class II HLA-DRB1 with TB susceptibility and valuable marker for disease development especially in Asian populations. Case-control studies have found the association of HLA-DR2 in some populations, but not in other populations, this could be due to an ethnic specific association of gene variants. Recently, GWAS conducted in case-control and family based studies in Russia, Chinese Han, Morocco, Uganda and Tanzania revealed the association of genes such as ASAP1, Alkylglycerol monooxygenase (AGMO), Forkhead BoxP1 (FOXP1), C-terminal domain phosphatase 1 (UBLCP1) and intergenic SNP rs932347C/T with TB. Whereas, SNP rs10956514A/G were not associated with TB in western Chinese Han and Tibetan population. In this review, we summarize the recent findings of genetic variants with susceptibility/resistance to TB.

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Section: Genetic Variants and Tb Associationsupporting

confidence: 80%

Influence of Genetic Polymorphism Towards Pulmonary Tuberculosis Susceptibility

2018

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“…We hypothesize that different allelic frequencies in genes that are crucial at a number of stages in the immune defence against Mtb will impact the host resistance to this infection and its progression. Within an admixed population such as that investigated here, there will be a wide variety of susceptibility alleles, some derived from different ancestral input [ 15 , 16 , 17 ] and others representing normal variation in any population [ 18 , 19 , 20 , 21 ]. Resistance to TB may encompass resistance to infection, or resistance to progression of disease, and our linkage studies in this community show that two separate loci are involved [ 22 ], and we postulated that patients who maintain a zero measure for skin test positivity, are inherently resistant.…”

Section: Discussionmentioning

confidence: 99%

The Risk of Tuberculosis Reinfection Soon after Cure of a First Disease Episode Is Extremely High in a Hyperendemic Community

et al. 2015

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Elevated rates of reinfection tuberculosis in various hyperendemic regions have been reported and, in particular, it has been shown that in a high-incidence setting near Cape Town, South Africa, the rate of reinfection tuberculosis (TB) disease after cure of a previous TB disease episode is about four times greater than the rate of first-time TB disease. It is not known whether this elevated rate is caused by a high reinfection rate due, for instance, to living circumstances, or a high rate of progress to disease specific to the patients, or both. In order to address that question we analysed an extensive data set from clinics attended by TB patients in the high-incidence setting near Cape Town, South Africa and found that, in fact, the (average) rate of reinfection (as opposed to the rate of reinfection disease) after cure of a previous TB disease episode is initially about 0.85 per annum. This rate diminishes rapidly over time and after about ten years this rate is similar to the rate of infection in the general population. Also, the rate of progress to disease after reinfection is initially high but declines in subsequent years down to the figure typical for the general population. These findings suggest that the first few months after cure of a TB disease episode form a critical period for controlling reinfection disease in a hyperendemic setting and that monitoring such cured patients could pre-empt a reinfection progressing to active disease.

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“…In fact, there is a higher prevalence of the KIR group A haplotype (expressing more inhibitory KIR) among patients with active tuberculosis when compared with resistant individuals. Indeed, certain KIR genes have increased correlation with the likelihood to become ill (i.e., KIR3DL1, KIR2DL3, KIR2DS1, and KIR2DS5), whereas others associate with a protective phenotype (i.e., KIR3DS1, KIR2DS2) ( 58 – 61 ). Portevin et al confirmed these observations by demonstrating NK cells from healthy individuals’ respond to direct contact with Mtb and M. bovis BCG and that the degree of such responses was dependent on the KIR haplotype.…”

Section: Role Of Nk Cells In the Immune Response Against Mmentioning

confidence: 99%

Memory of Natural Killer Cells: A New Chance against Mycobacterium tuberculosis?

et al. 2017

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Natural killer (NK) cells are lymphocytes of the innate immune system, which play an important role in the initial defense against a wide variety of pathogens, including viruses and intracellular bacteria. NK cells produce cytokines that enhance immune responses directed toward pathogens and also exert cytotoxic activity against infected cells, thereby eliminating the reservoir of infection. Their role in defense against Mycobacterium tuberculosis (Mtb) has been recently studied, and there is increasing evidence that highlight the importance of NK cell function during pulmonary tuberculosis (PTB), especially in the absence of optimal T-cell responses. Additionally, in the last years, it has been observed that NK cells mediate secondary responses against antigens to which they were previously exposed, an ability classically attributed to lymphocytes of the adaptive branch of immunity. This phenomenon, called “innate memory,” could have important implications in the efforts to develop therapies and vaccines to improve the initial phases of immune reactions against different microorganisms, especially those to which there is not yet available vaccines to prevent infection, as is the case for tuberculosis. Therefore, the possibility of inducing memory-like NK cells ready to act prior to contact with Mtb or during the earliest stages of infection becomes quite interesting. However, our understanding of the mechanisms of innate memory remains incomplete. Here, we review recent literature about the mechanisms involved in the formation and maintenance of NK cell memory and the role of these cells in the immune response during tuberculosis. Finally, we discuss if the current evidence is sufficient to substantiate that NK cells exert more rapid and robust secondary responses after consecutive encounters with Mtb.

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Activating KIRs alter susceptibility to pulmonary tuberculosis in a South African population

Cited by 20 publications

References 24 publications

Influence of Genetic Polymorphism Towards Pulmonary Tuberculosis Susceptibility

Influence of Genetic Polymorphism Towards Pulmonary Tuberculosis Susceptibility

The Risk of Tuberculosis Reinfection Soon after Cure of a First Disease Episode Is Extremely High in a Hyperendemic Community

Memory of Natural Killer Cells: A New Chance against Mycobacterium tuberculosis?

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