Analysis of Th1, Th17 and regulatory T cells in tuberculosis case contacts

García-Jacobo, R.E.; Serrano, Carmen; Moreno, José María Villagrán; Ramírez, O. Gaspar; Trujillo-Ochoa, Jorge L; Uresti-Rivera, Edith Elena; Portales-Pérez, Diana Patricia; González‐Amaro, Roberto; Hernández, Manuel Hernández

doi:10.1016/j.cellimm.2014.03.010

Cited by 21 publications

(10 citation statements)

References 42 publications

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“…In vitro treatment with a PD1 mAb of cell cultures derived from patients with TB reduced immunosuppression by blocking T cell apoptosis, restoring IFNγ production and triggering IFNγ-dependent killing of Mtb-infected macrophages 122,123 . Similarly, the increased surface expression of CTLA4 has also been reported in TB 121,126,127 , and the checkpoint receptor LAG3 was found to be highly expressed by CD4 + T cells and NK cells in the lungs of non-human primates that progressed to active TB, but not in animals with LTBI 128 . This observation suggests that changes in LAG3 expression patterns influence disease outcome and Mtb replication.…”

Section: Signalling Via Pd1 Inhibits T Cell Proliferation Andmentioning

confidence: 53%

Host-directed therapies for bacterial and viral infections

Kaufmann

Dorhoi

Hotchkiss

et al. 2017

Nat Rev Drug Discov

568

440

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Despite the recent increase in the development of antivirals and antibiotics, antimicrobial resistance and the lack of broad-spectrum virus-targeting drugs are still important issues and additional alternative approaches to treat infectious diseases are urgently needed. Host-directed therapy (HDT) is an emerging approach in the field of anti-infectives. The strategy behind HDT is to interfere with host cell factors that are required by a pathogen for replication or persistence, to enhance protective immune responses against a pathogen, to reduce exacerbated inflammation and to balance immune reactivity at sites of pathology. Although HDTs encompassing interferons are well established for the treatment of chronic viral hepatitis, novel strategies aimed at the functional cure of persistent viral infections and the development of broad-spectrum antivirals against emerging viruses seem to be crucial. In chronic bacterial infections, such as tuberculosis, HDT strategies aim to enhance the antimicrobial activities of phagocytes and to curtail inflammation through interference with soluble factors (such as eicosanoids and cytokines) or cellular factors (such as co-stimulatory molecules). This Review describes current progress in the development of HDTs for viral and bacterial infections, including sepsis, and the challenges in bringing these new approaches to the clinic.

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Section: Signalling Via Pd1 Inhibits T Cell Proliferation Andmentioning

confidence: 53%

Host-directed therapies for bacterial and viral infections

Kaufmann

Dorhoi

Hotchkiss

et al. 2017

Nat Rev Drug Discov

568

440

View full text Add to dashboard Cite

show abstract

“…Anti‐inflammatory cytokines produced in granulomas, such as IL‐27, IL‐10, and TGF‐β, can act on T cells. Other cells that participate in anti‐inflammatory responses to Mtb include TH17 cells, regulatory T cells (Tregs, CD4+Foxp3+ T cells), and neutrophils . There are limited data on the role of these cell subsets in Mtb infection.…”

Section: Experimental Support For a Balanced Response In Tbmentioning

confidence: 99%

Dynamic balance of pro‐ and anti‐inflammatory signals controls disease and limits pathology

Cicchese

Evans

Hult

et al. 2018

Immunological Reviews

235

171

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Immune responses to pathogens are complex and not well understood in many diseases, and this is especially true for infections by persistent pathogens. One mechanism that allows for long-term control of infection while also preventing an over-zealous inflammatory response from causing extensive tissue damage is for the immune system to balance pro- and anti-inflammatory cells and signals. This balance is dynamic and the immune system responds to cues from both host and pathogen, maintaining a steady state across multiple scales through continuous feedback. Identifying the signals, cells, cytokines, and other immune response factors that mediate this balance over time has been difficult using traditional research strategies. Computational modeling studies based on data from traditional systems can identify how this balance contributes to immunity. Here we provide evidence from both experimental and mathematical/computational studies to support the concept of a dynamic balance operating during persistent and other infection scenarios. We focus mainly on tuberculosis, currently the leading cause of death due to infectious disease in the world, and also provide evidence for other infections. A better understanding of the dynamically balanced immune response can help shape treatment strategies that utilize both drugs and host-directed therapies.

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“…changing dynamics of infection and control of bacterial load. In a comparison of T-cell subsets between IGRA-consistently positive and consistently negative TB-case contacts, CD4 + Foxp3 + and CD4 + CTLA-4 + Tregs were increased in TB-case contacts with consistently positive IGRA-tests, possibly indicating Treg interference with host resistance in the development of active infection ( 121 ).…”

Section: Tregs In Leprosy and Tuberculosismentioning

confidence: 99%

Regulatory T-Cells at the Interface between Human Host and Pathogens in Infectious Diseases and Vaccination

2015

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Regulatory T-cells (Tregs) act at the interface of host and pathogen interactions in human infectious diseases. Tregs are induced by a wide range of pathogens, but distinct effects of Tregs have been demonstrated for different pathogens and in different stages of infection. Moreover, Tregs that are induced by a specific pathogen may non-specifically suppress immunity against other microbes and parasites. Thus, Treg effects need to be assessed not only in homologous but also in heterologous infections and vaccinations. Though Tregs protect the human host against excessive inflammation, they probably also increase the risk of pathogen persistence and chronic disease, and the possibility of disease reactivation later in life. Mycobacterium leprae and Mycobacterium tuberculosis, causing leprosy and tuberculosis, respectively, are among the most ancient microbes known to mankind, and are master manipulators of the immune system toward tolerance and pathogen persistence. The majority of mycobacterial infections occur in settings co-endemic for viral, parasitic, and (other) bacterial coinfections. In this paper, we discuss recent insights in the activation and activity of Tregs in human infectious diseases, with emphasis on early, late, and non-specific effects in disease, coinfections, and vaccination. We highlight mycobacterial infections as important models of modulation of host responses and vaccine-induced immunity by Tregs.

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Analysis of Th1, Th17 and regulatory T cells in tuberculosis case contacts

Cited by 21 publications

References 42 publications

Host-directed therapies for bacterial and viral infections

Host-directed therapies for bacterial and viral infections

Dynamic balance of pro‐ and anti‐inflammatory signals controls disease and limits pathology

Regulatory T-Cells at the Interface between Human Host and Pathogens in Infectious Diseases and Vaccination

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