Regulation of Interferon-γ receptor (IFN-γR) expression in macrophages during Mycobacterium tuberculosis infection

Kak, Gunjan; Tiwari, Brijendra K; Singh, Yogendra; Natarajan, Krishnamurthy

doi:10.1515/bmc-2020-0006

Cited by 8 publications

(4 citation statements)

References 23 publications

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“…Since IFN-γ plays a critical role in the host protective response against mycobacteria, blocking IFN-γR mediated signaling is believed to be an important Mtb evasion strategy [80]. IFN-γR gene knockout mice or mice having genetic defects in IFN-γR were occurred to be extremely susceptible to Mtb infection [81].…”

Section: Interferon (Ifn)-gamma (γ) Receptor (Ifn-γr)mentioning

confidence: 99%

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Cytokine Receptors—Regulators of Antimycobacterial Immune Response

Druszczyńska

Godkowicz

Kulesza

et al. 2022

IJMS

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Cytokine receptors are critical regulators of the antimycobacterial immune response, playing a key role in initiating and coordinating the recruitment and activation of immune cells during infection. They recognize and bind specific cytokines and are involved in inducing intracellular signal transduction pathways that regulate a diverse range of biological functions, including proliferation, differentiation, metabolism and cell growth. Due to mutations in cytokine receptor genes, defective signaling may contribute to increased susceptibility to mycobacteria, allowing the pathogens to avoid killing and immune surveillance. This paper provides an overview of cytokine receptors important for the innate and adaptive immune responses against mycobacteria and discusses the implications of receptor gene defects for the course of mycobacterial infection.

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Section: Interferon (Ifn)-gamma (γ) Receptor (Ifn-γr)mentioning

confidence: 99%

“…The resulting phenotype made macrophages resistant to the protective effect of IFN-γ, despite its presence at optimal levels [83]. [80]. IFN-γR gene knockout mice or mice having genetic defects in IFN-γR were occurred to be extremely susceptible to Mtb infection [81].…”

Section: Interferon (Ifn)-gamma (γ) Receptor (Ifn-γr)mentioning

confidence: 99%

Cytokine Receptors—Regulators of Antimycobacterial Immune Response

Druszczyńska

Godkowicz

Kulesza

et al. 2022

IJMS

View full text Add to dashboard Cite

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“…IFN-γ has been repeatedly proven to be crucial in host defense TB ( 25 ). IFN-γ pathway defects are accompanied by increased susceptibility to low-virulence mycobacterium infections.…”

Section: Discussionmentioning

confidence: 99%

The regulation and potential role of interleukin-32 in tuberculous pleural effusion

Wang,

Yang,

Quan

et al. 2024

Front. Immunol.

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The possible protective effect of interleukin-32 (IL-32) in Mycobacterium tuberculosis (Mtb) infection has been indicated. However, few studies have been focused on IL-32 in tuberculosis patients. Additionally, the regulation of IL-32 production has rarely been reported. In the present study, the production, regulation, and role of IL-32 in tuberculous pleurisy (TBP) were investigated. We found that the content of IL-32 in tuberculous pleural effusion (TPE) was higher than the level in the malignant pleural effusion and transudative pleural effusion. The level of IL-32 mRNA in pleural fluid mononuclear cells (PFMCs) was higher than that in peripheral blood mononuclear cells (PBMCs) of patients with TBP, and this difference was mainly reflected in the splice variants of IL-32α, IL-32β, and IL-32γ. Compared with the PBMCs, PFMCs featured higher IL-32β/IL-32γ and IL-32α/IL-32γ ratios. In addition, lipopolysaccharide (LPS), Bacillus Calmette-Guérin (BCG), and H37Ra stimulation could induce IL-32 production in the PFMCs. IL-32 production was positively correlated with the TNF-α, IFN‐γ, and IL-1Ra levels in TPE, whereas IFN-γ, but not TNF-α or IL-1Ra, could induce the production of IL-32 in PFMCs. Furthermore, IL-32γ could induce the TNF-α production in PFMCs. Monocytes and macrophages were the main sources of IL-32 in PFMCs. Nevertheless, direct cell–cell contact between lymphocytes and monocytes/macrophages plays an important role in enhancing IL-32 production by monocyte/macrophage cells. Finally, compared with the non-tuberculous pleural effusion, the purified CD4+ and CD8+ T cells in TPE expressed higher levels of intracellular IL-32. Our results suggested that, as a potential biomarker, IL-32 may play an essential role in the protection against Mtb infection in patients with TBP. However, further studies need to be carried out to clarify the functions and mechanisms of the IFN-γ/IL-32/TNF-α axis in patients with TBP.

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“…This may be attributed to that poor glycemic control impedes the activation of alveolar macrophages, leading to inadequate phagocytosis of Mycobacterium tuberculosis [ 8 , 25 ]. Patients with poor glycemic control were also found to have lower levels of IFN- γ [ 26 ], which is considered to be closely associated with the prognosis of tuberculosis [ 27 ]. Therefore, glycemic control in diabetes-tuberculosis treatment should be paid considerable attention.…”

Section: Discussionmentioning

confidence: 99%

Interaction of Glycemic Control and Statin Use on Diabetes‐Tuberculosis Treatment Outcome: A Nested Case‐Control Study

Meng,

Zheng,

et al. 2024

Canadian Journal of Infectious Diseases and Medical Microbiolog

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This study aims to explore the interaction of glycemic control and statin use on the treatment outcomes of pulmonary tuberculosis‐diabetes comorbidity (PTB‐DM) patients. A nested case‐control study was conducted in a tuberculosis patients’ cohort. We defined cases as patients who experienced unfavorable outcomes. Glycemic control was estimated at the baseline. Statin use was obtained from medical records. The multivariate logistic regression models were developed, and the interaction table invented by Andersson was adopted to analyze the interaction of glycemic control and statin use on treatment outcomes. A total of 2,047 patients were included in this study. There was a significant interaction between glycemic control and statin use on the treatment outcomes. Patients with good glycemic control and no statin use (OR = 0.464, 95% CI: 0.360–0.623) had a lower risk of unfavorable outcomes than those with poor glycemic control and statin use (OR = 0.604, 95% CI: 0.401–0.734). Patients with good glycemic control and statin use had the lowest risk of unfavorable outcomes (OR = 0.394, 95% CI: 0.264–0.521). Glycemic control in diabetes‐tuberculosis treatment should be paid considerable attention. Patients can benefit from statin use even if they have poor glycemic control. Patients with good glycemic control and statin use can have the best outcomes.

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Regulation of Interferon-γ receptor (IFN-γR) expression in macrophages during Mycobacterium tuberculosis infection

Cited by 8 publications

References 23 publications

Cytokine Receptors—Regulators of Antimycobacterial Immune Response

Cytokine Receptors—Regulators of Antimycobacterial Immune Response

The regulation and potential role of interleukin-32 in tuberculous pleural effusion

Interaction of Glycemic Control and Statin Use on Diabetes‐Tuberculosis Treatment Outcome: A Nested Case‐Control Study

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