Impaired NK cells' activity and increased numbers of CD4 + CD25+ regulatory T cells in multidrug-resistant Mycobacterium tuberculosis patients

Fan, Renhua; Xiang, Yong‐Bing; Li, Yang; Liu, Yanke; Chen, Pingsheng; Wang, Lei; Feng, Wenjun; Yin, Kai; Fu, Manjiao; Xu, Yixin; Wu, Jialin

doi:10.1016/j.tube.2016.02.001

Cited by 16 publications

(17 citation statements)

References 29 publications

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“…The same differences were found when looking at CD4 + CD25 + cells expressing the co-stimulatory receptors PD-1 or CTLA-4. Similarly, patients with MDR-TB had higher (though not significantly higher) percentages of CD4 + CD25 + Tregs in blood and higher IL-10 levels in serum than those with drug-sensitive TB (80). We note that neither of these studies provided any data on the extent of pulmonary disease, which usually is worse in MDR-TB (81).…”

Section: Tregs and Diseasementioning

confidence: 96%

Regulatory T Cells in Mycobacterium tuberculosis Infection

Cardona

2019

Front. Immunol.

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Anti-inflammatory regulatory T cells have lately attracted attention as part of the immune response to Mycobacterium tuberculosis infection, where they counterbalance the protective but pro-inflammatory immune response mediated by Th17 cells and especially by the better-known Th1 cells. In chronic infectious diseases there is a delicate balance between pro- and anti-inflammatory responses. While Th1 and Th17 are needed in order to control infection by Mycobacterium tuberculosis, the inflammatory onset can ultimately become detrimental for the host. In this review, we assess current information on the controversy over whether counterbalancing regulatory T cells are promoting pathogen growth or protecting the host.

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Section: Tregs and Diseasementioning

confidence: 96%

Regulatory T Cells in Mycobacterium tuberculosis Infection

Cardona

2019

Front. Immunol.

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“…As an example, CD4 + Tregs were isolated and correlated with apoptotic activity from human lepromatous leprosy patients [159]. In addition, patients with active TB were found to have increased frequencies of CD4 + Tregs producing IL-10 [56]. In a mouse model of Leishmania donovani infection, CD4 + Foxp3 + Tregs play an important role in delaying the development of splenic pathology and restricting leukocyte expansion [57].…”

Section: Host Defense Against Microbial Infectionsmentioning

confidence: 99%

Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies

Thakur

Mikkelsen

Jungersen

2019

Journal of Immunology Research

246

185

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Infectious diseases caused by pathogens including viruses, bacteria, fungi, and parasites are ranked as the second leading cause of death worldwide by the World Health Organization. Despite tremendous improvements in global public health since 1950, a number of challenges remain to either prevent or eradicate infectious diseases. Many pathogens can cause acute infections that are effectively cleared by the host immunity, but a subcategory of these pathogens called “intracellular pathogens” can establish persistent and sometimes lifelong infections. Several of these intracellular pathogens manage to evade the host immune monitoring and cause disease by replicating inside the host cells. These pathogens have evolved diverse immune escape strategies and overcome immune responses by residing and multiplying inside host immune cells, primarily macrophages. While these intracellular pathogens that cause persistent infections are phylogenetically diverse and engage in diverse immune evasion and persistence strategies, they share common pathogen type-specific mechanisms during host-pathogen interaction inside host cells. Likewise, the host immune system is also equipped with a diverse range of effector functions to fight against the establishment of pathogen persistence and subsequent host damage. This article provides an overview of the immune effector functions used by the host to counter pathogens and various persistence strategies used by intracellular pathogens to counter host immunity, which enables their extended period of colonization in the host. The improved understanding of persistent intracellular pathogen-derived infections will contribute to develop improved disease diagnostics, therapeutics, and prophylactics.

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“…However, in patients with active PTB, there is reduced frequency of CD56 bright cells in the peripheral leukocyte population, accompanied by decreased expression of NK cell activating receptors (NKp30, NKp46), resulting in declined functional capacity ( 64 , 65 ). This functional impairment of NK cells is also associated with an increase in CD4 + CD25 + regulatory T cells (T reg ), which may regulate the activity of NK cells ( 66 ). It is unknown if such alterations in NK cell functionality are related to the risk of bacterial dissemination to extrapulmonary sites.…”

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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Impaired NK cells' activity and increased numbers of CD4 + CD25+ regulatory T cells in multidrug-resistant Mycobacterium tuberculosis patients

Cited by 16 publications

References 29 publications

Regulatory T Cells in Mycobacterium tuberculosis Infection

Regulatory T Cells in Mycobacterium tuberculosis Infection

Intracellular Pathogens: Host Immunity and Microbial Persistence Strategies

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

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