T cells and their immunometabolism: A novel way to understanding sepsis immunopathogenesis and future therapeutics

Kumar, Vijay

doi:10.1016/j.ejcb.2018.05.001

Cited by 87 publications

(71 citation statements)

References 261 publications

(335 reference statements)

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“…41 Besides the numerical loss or clonal shift, multiple dysfunctions in T cells' metabolism and activation in sepsis have been reported. 44 Nonetheless, the extent to which these cell-intrinsic impairments contribute to post-sepsis immunosuppression has now been challenged, 45,46 implying a prominent role of T cells' extrinsic cues in the post-sepsis environment (eg, defective antigen presentation). Also, the impact of sepsis on non-conventional, but biologically potent T-cell subsets such natural killer T cells or γδ T cells deserves more attention.…”

Section: Immunological Gaps During Sepsismentioning

confidence: 99%

Current gaps in sepsis immunology: new opportunities for translational research

Rubio

Osuchowski

Shankar-Hari

et al. 2019

The Lancet Infectious Diseases

250

207

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Increasing evidence supports a central role of the immune system in sepsis, but the current view of how sepsis affects immunity, and vice versa, is still rudimentary. The European Group on Immunology of Sepsis has identified major gaps that should be addressed with high priority, such as understanding how immunological alterations predispose to sepsis, key aspects of the immunopathological events during sepsis, and the long-term consequences of sepsis on patient's immunity. We discuss major unmet topics in those three categories, including the role of key immune cells, the cause of lymphopenia, organ-specific immunology, the dynamics of sepsis-associated immunological alterations, the role of the microbiome, the standardisation of immunological tests, the development of better animal models, and the opportunities offered by immunotherapy. Addressing these gaps should help us to better understand sepsis physiopathology, offering translational opportunities to improve its prevention, diagnosis, and care.

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Section: Immunological Gaps During Sepsismentioning

confidence: 99%

Current gaps in sepsis immunology: new opportunities for translational research

Rubio

Osuchowski

Shankar-Hari

et al. 2019

The Lancet Infectious Diseases

250

207

View full text Add to dashboard Cite

show abstract

“…The mortality of ALI caused by sepsis may be as high as 80% if it is not diagnosed and treated early Th17 cell is shown to be involved in its occurrence and development [19,20]. Since Th17 and Th22 both belong to T helper cell subsets, it is likely that Th22 cells play regulatory role in sepsis-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

Increased Th17 and Th22 cell levels predict acute lung injury in patients with sepsis

Zhang²,

Han

et al. 2019

Preprint

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Background: Acute lung injury (ALI) is one of the major complications of severe sepsis. This study was conducted to investigate the levels of Th22 and Th17 cells in the peripheral blood septic patients with ALI and their clinical significance. Results: A total of 479 septic patients admitted between January 2013 to January 2018 were divided into non-ALI (n = 377) and ALI groups (n = 102) based on the presence or absence of ALI. The levels of Th22 and Th17 cells, interleukin 22 (IL-22), 6 (IL-6) and 17 (IL-17) were determined. Receiver operating characteristic curve (ROC) analysis was performed to assess the early diagnostic value of Th22 and Th17 cells to predict sepsis-induced ALI. The lung injury prediction score (LIPS), IL-6, IL-17, IL-22, and levels of Th17 and Th-22 cells were 9.13, 14.02 ng/L, 13.06 ng/L, 22.90 ng/L, 8.80% and 7.40%, respectively, in the ALI patients and were significantly higher in the ALI group than in non-ALI group (P < 0.05). Pearson correlation analysis showed that LIPS, IL-17, IL-22, Th17 cells and Th22 cells were significant factors affecting sepsis-induced ALI (P < 0.05). The correlation analysis showed that the levels of Th22 cells in the peripheral blood of septic patients with ALI were positively correlated with LIPS, IL-22 and the levels of Th17 cells (P < 0.05), and the levels of Th17 cells were positively correlated with LIPS and IL-17 (P < 0.01). Multivariate logistic regression analysis showed that the LIPS (OR = 1.130), IL-17 (OR = 1.982), IL-22 (OR =2.612) and levels of Th17 (OR = 2.211) and Th22 (OR =3.230) cells were independent risk factor for ALI. The area under the curve of Th22 cells was 0.844 with a cutoff value of 6.81% to predict ALI. The sensitivity and specificity for early diagnosis of sepsis-induced ALI by Th22 cells were 78.72% and 89.13% respectively, which were better but statistically similar as compared with Th17 cells (P > 0.05). Conclusions: The levels of Th22 and Th17 cells in peripheral blood are significantly increased in septic patients with induced ALI, and may be used for early diagnose of sepsis-induced ALI.

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“…The metabolic reprogramming among immune cells (macrophages, neutrophils, DC, T cells, and NK cells) or immunometabolism plays a critical in role the pathogenesis of inflammation and other inflammatory diseases, including sepsis where the cytokine storm generation plays a significant role in the induction of ALI/ARDS or multiple organ failure [17,[135][136][137][138][139]. Hence, it also becomes crucial to observe immunometabolic re-programming among both, innate and adaptive immune cells during the SARS-CoV2 pathogenesis.…”

Section: Metabolic Reprogramming Among Immune Cells During Covid-19mentioning

confidence: 99%

“…T cells under normal conditions called quiescent or naïve T (Tn) cells depend on OXPHOS for their energy demand ( Figure 6) [138]. The pyruvate required for OXPHOS comes from glycolysis, FAO, and glutaminolysis under the influence of tonic TCR signaling and IL-7-IL-7R interaction to maintain growth, differentiation, survival, activation, and function ( Figure 6) [138]. S1P-S1PR interaction also promotes Tn cell survival via maintaining OXPHOS and FAO ( Figure 6) [224].…”

Section: Immunometabolic Programing Among T and B Cells During Sars-cmentioning

confidence: 99%

How could we forget immunometabolism in SARS-CoV2 infection or COVID-19?

Kumar

2020

International Reviews of Immunology

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SARS-CoV2 infection or COVID-19 has created panic around the world since its first origin in December 2019 in Wuhan city, China. The COVID-19 pandemic has infected more than 46.4 million people, with 1,199,727 deaths. The immune system plays a crucial role in the severity of COVID-19 and the development of pneumonia-induced acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). Along with providing protection, both innate and T cell-based adaptive immune response dysregulate during severe SARS-CoV2 infection. This dysregulation is more pronounced in older population and patients with comorbidities (Diabetes, hypertension, obesity, other pulmonary and autoimmune diseases). However, COVID-19 patients develop protective antibodies (Abs) against SARS-CoV2, but they do not long for last. The induction of the immune response against the pathogen also requires metabolic energy that generates through the process of immunometabolism. The change in the metabolic stage of immune cells from homeostasis to an inflammatory or infectious environment is called immunometabolic reprogramming. The article describes the cellular immunology (macrophages, T cells, B cells, dendritic cells, NK cells and pulmonary epithelial cells (PEC) and vascular endothelial cells) and the associated immune response during COVID-19. Immunometabolism may serve as a cell-specific therapeutic approach to target COVID-19.

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T cells and their immunometabolism: A novel way to understanding sepsis immunopathogenesis and future therapeutics

Cited by 87 publications

References 261 publications

Current gaps in sepsis immunology: new opportunities for translational research

Current gaps in sepsis immunology: new opportunities for translational research

Increased Th17 and Th22 cell levels predict acute lung injury in patients with sepsis

How could we forget immunometabolism in SARS-CoV2 infection or COVID-19?

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