Programmed Death Ligand 1 on <i>Burkholderia pseudomallei</i>–Infected Human Polymorphonuclear Neutrophils Impairs T Cell Functions

Buddhisa, Surachat; Rinchai, Darawan; Ato, Manabu; Bancroft, Gregory J.; Lertmemongkolchai, Ganjana

doi:10.4049/jimmunol.1402417

Cited by 30 publications

(28 citation statements)

References 42 publications

(58 reference statements)

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“…These neutrophils suppress T cell function via PD-L1/PD-1 interaction and production of ROS [89]. The same suppressive function was also observed in Burkholderia pseudomallei infected neutrophils, that up-regulated expression of PD-L1 and was able to inhibit CD4 + T cell proliferation and IFN-γ production in response to polyclonal activators, mediated by the PD-L1/PD-1 pathway [90].…”

Section: T Cell Activities Under Neutrophils Controlsupporting

confidence: 54%

Neutrophils Plasticity: The Regulatory Interface in Various Pathological Conditions

Perobelli¹,

Silva²,

AdrianaBonomo³

2017

Role of Neutrophils in Disease Pathogenesis

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It is now known that neutrophils make up a population of complex cells with great plasticity, challenging the old view of neutrophil association with tissue damage and early phases of infection. Here, we discuss different contexts in which these cells can induce anti-inflammatory responses. Although distinct surface markers and cytokines profiles were shown, the most reliable characterization of suppressor neutrophil subtypes relies on their functional characteristics. One important example of inhibitory neutrophils generation comes from in vivo treatment with G-CSF, for 5 days, as for hematopoieticstem-cell-transplantation (HSCT). In this case,donor blood is enriched in degranulated granulocytes harboring a functional regulatory phenotype, characterized by IL-10 production. These cells, when transferred together with HSCT, are able to reduce graft-versus-host-disease, being influenced by Treg cells and influencing them back. Importantly, this protection is long lasting and specific, keeping immunocompetence to other antigens. This regulation is paramount in HSCT, and represents a simple approach to be applied in humans. In summary, we discuss the interaction of neutrophils with other cell types and its consequence in immunomodulation. We believe these features confer an important bridge between innate and adaptive immune system, building a new knowledge for an underestimated cell type.

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Section: T Cell Activities Under Neutrophils Controlsupporting

confidence: 54%

Neutrophils Plasticity: The Regulatory Interface in Various Pathological Conditions

Perobelli¹,

Silva²,

AdrianaBonomo³

2017

Role of Neutrophils in Disease Pathogenesis

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“…In addition, the exhausted CD8+ T cell population also expressed inhibitor receptors, such as PD-1 and lymphocyte activation gene 3. In an in vitro study on the effect of B. pseudomallei K96243 on human polymorphonuclear neutrophils (PMNs) and CD4+ T cell function, it was found that there was a greater inhibition of T cell functions (proliferation and IFN-γ expression) by infected B. pseudomallei PMNs than by uninfected PMNs [60]. It was also reported that T cell suppression caused by infected PMNs was mediated by the programmed death 1 (PD-1)/programmed death ligand-1 (PD-L1) pathway.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of TNF-α and IFN-γ expression is a common host immune response in a chronically infected mouse model of melioidosis when comparing multiple human strains of Burkholderia pseudomallei

et al. 2020

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Background: Melioidosis is endemic in Southeast Asia and Northern Australia and is caused by the Gram-negative, facultative intracellular pathogen Burkholderia pseudomallei. Diagnosis of melioidosis is often difficult because of the protean clinical presentation of the disease, and it may mimic other diseases, such as tuberculosis. There are many different strains of B. pseudomallei that have been isolated from patients with melioidosis, but it was not clear if they could cause a similar disease in a chronic BALB/c murine model of melioidosis. Hence, we wanted to examine chronically infected mice exposed to different strains of B. pseudomallei to determine if there were differences in the host immune response to the pathogen. Results:We identified common host immune responses exhibited in chronically infected BALB/c mice, although there was some heterogeneity in the host response in chronically infected mice after exposure to different strains of B. pseudomallei. They all displayed pyogranulomatous lesions in their spleens with a large influx of monocytes/ macrophages, NK cells, and neutrophils identified by flow cytometry. Sera from chronically infected mice by ELISA exhibited elevated IgG titers to the pathogen, and we detected by Luminex micro-bead array technology a significant increase in the expression of inflammatory cytokines/chemokines, such as IFN-γ, IL-1α, IL-1β, KC, and MIG. By immunohistochemical and in situ RNA hybridization analysis we found that the increased expression of proinflammatory cytokines (IL-1α, IL-1β, TNF-α, IFN-γ) was confined primarily to the area with the pathogen within pyogranulomatous lesions. We also found that cultured splenocytes from chronically infected mice could express IFN-γ, TNF-α, and MIP-1α ex vivo without the need for additional exogenous stimulation. In addition by flow cytometry, we detected significant amounts of intracellular expression of TNF-α and IFN-γ without a protein transport blocker in monocytes/macrophages, NK cells, and neutrophils but not in CD4 + or CD8 + T cells in splenocytes from chronically infected mice.

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“…Another crucial issue is that the definition of ‘immunosuppressive’ must rely on the demonstrated capacity to suppress T‐cell responses (such as proliferation and/or IFN‐ γ production) by neutrophils . The inhibition of T‐cell responses by human immunosuppressive neutrophils primarily occurs through an overproduction of ARG‐1, ROS, or via PD‐L1‐dependent interactions . Polarization of T‐helper cell responses towards an anti‐inflammatory phenotype (expansion of Th2 and Treg cells and inhibition of Th1 cells) has also been proposed as an immunosuppressive mechanism used by human LDNs/PMN‐MDSCs .…”

Section: Neutrophils and T Cellsmentioning

confidence: 99%

Recent advances on the crosstalk between neutrophils and B or T lymphocytes

et al. 2018

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An increasing body of literature supports a role for neutrophils as players in the orchestration of adaptive immunity. During acute and chronic inflammatory conditions, neutrophils rapidly migrate not only to sites of inflammation, but also to draining lymph nodes and spleen, where they engage bidirectional interactions with B-and T-lymphocyte subsets. Accordingly, a relevant role of neutrophils in modulating B-cell responses under homeostatic conditions has recently emerged. Moreover, specialized immunoregulatory properties towards B or T cells acquired by distinct neutrophil populations, originating under pathological conditions, have been consistently described. In this article, we summarize the most recent data from human studies and murine models on the ability of neutrophils to modulate adaptive immune responses under physiological and pathological conditions and the mechanisms behind these processes.

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Programmed Death Ligand 1 on Burkholderia pseudomallei–Infected Human Polymorphonuclear Neutrophils Impairs T Cell Functions

Cited by 30 publications

References 42 publications

Neutrophils Plasticity: The Regulatory Interface in Various Pathological Conditions

Neutrophils Plasticity: The Regulatory Interface in Various Pathological Conditions

Dysregulation of TNF-α and IFN-γ expression is a common host immune response in a chronically infected mouse model of melioidosis when comparing multiple human strains of Burkholderia pseudomallei

Recent advances on the crosstalk between neutrophils and B or T lymphocytes

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