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Programmed death ligand 1 on Burkholderia pseudomallei-infected human polymorphonuclear neutrophils impairs T cell
Surachat Buddhisa1, Darawan Rinchai1, Manabu Ato2
1Centre for Research and Development of Medical Diagnostic Laboratories, Faculty of Associated Medical Sciences, Khon Kaen University, Khon Kaen 40002, Thailand;
Abstract:
Polymorphonuclear neutrophils (PMNs) are terminally differentiated cells that are involved in innate immune responses and form an early line of defense against pathogens. More recently, it has been shown that PMNs have immunosuppressive abilities on other immune cells. However, the effect of PMNs on T cell responses during bacterial infection remains to be determined. In this report, we examined the interaction of PMNs and T cells in response to infection with Burkholderia pseudomallei, the causative agent of human melioidosis. We observed that CD4(+) T cell proliferation and IFN-γ production in response to polyclonal activators is significantly inhibited by uninfected PMNs, and to a greater extent B. pseudomallei-infected PMNs. Programmed death ligand 1 (PD-L1), a known regulator of T cell activation, is increased in mRNA expression in the blood of patients and upon infection of PMNs in vitro. The increased expression of PD-L1 was correlated with the degree of T cell inhibition in individuals with type 2 diabetes, a major risk factor of melioidosis. In vitro, addition of anti-PD-L1 Abs blocked this inhibitory activity and restored proliferation of CD4(+) T cells and IFN-γ production, suggesting that PD-L1 on B. pseudomallei-infected PMNs is a regulatory molecule for the functions of T cells and may be involved in pathogenesis versus control of melioidosis.
Insights
Polymorphonuclear neutrophils (PMNs) suppress T cell responses during bacterial infection. Programmed death ligand 1 (PD-L1) on infected PMNs inhibits T cell proliferation and IFN-γ production, impacting melioidosis.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Polymorphonuclear neutrophils (PMNs) are crucial for innate immunity and pathogen defense.
- Emerging evidence suggests PMNs possess immunosuppressive capabilities.
- The impact of PMNs on T cell responses during bacterial infections requires further investigation.
Purpose of the Study:
- To investigate the interaction between PMNs and T cells during Burkholderia pseudomallei infection.
- To determine the role of PMNs in modulating T cell responses in melioidosis.
Main Methods:
- Examined PMN-T cell interactions in response to B. pseudomallei infection.
- Assessed CD4(+) T cell proliferation and IFN-γ production.
- Measured Programmed Death Ligand 1 (PD-L1) mRNA expression in patients and in vitro.
- Utilized anti-PD-L1 antibodies to block inhibitory activity.
Main Results:
- Uninfected and B. pseudomallei-infected PMNs significantly inhibited CD4(+) T cell proliferation and IFN-γ production.
- PD-L1 mRNA expression was elevated in patients' blood and in infected PMNs.
- Increased PD-L1 expression correlated with T cell inhibition in type 2 diabetes patients.
- Anti-PD-L1 antibodies restored T cell proliferation and IFN-γ production in vitro.
Conclusions:
- PMNs, particularly when infected with B. pseudomallei, suppress T cell responses.
- PD-L1 on infected PMNs is a key regulatory molecule mediating T cell inhibition.
- PD-L1-mediated immunosuppression by PMNs may contribute to melioidosis pathogenesis.
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