scholarly journals The role of tumor cells in the modification of T lymphocytes activity — the expression of the early CD69+, CD71+ and the late CD25+, CD26+, HLA/DR+ activation markers on T CD4+ and CD8+ cells in squamous cell laryngeal carcinoma. Part I

2012 ◽  
Vol 49 (4) ◽  
pp. 579-592 ◽  
Author(s):  
Katarzyna Starska ◽  
Ewa Głowacka ◽  
Andrzej Kulig ◽  
Iwona Lewy-Trenda ◽  
Magdalena Bryś ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Tumor Cells ◽  
Squamous Cell ◽  
Laryngeal Carcinoma ◽  
Activation Markers ◽  
Hla Dr

scholarly journals Preexisting Virus-Specific T Lymphocytes-Mediated Enhancement of Adenovirus Infections to Human Blood CD14+ Cells

Viruses ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 154
Author(s):  
Fengling Feng ◽  
Jin Zhao ◽  
Pingchao Li ◽  
Ruiting Li ◽  
Ling Chen ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Viral Infection ◽  
Viral Infections ◽  
Critical Role ◽  
Scavenger Receptor ◽  
Activation Markers ◽  
Gm Csf ◽  
Cell Responses ◽  
Underlying Mechanisms

Antigen-specific T lymphocytes play a critical role in controlling viral infections. However, we report here that preexisting virus-specific T cell responses also contribute to promoting adenovirus (Ad) infection. Previously, we found that CD14+ monocytes from Ad-seropositive individuals exhibited an increased susceptibility to Ad infection, when compared with that of Ad-seronegative individuals. But the underlying mechanisms for this enhancement of viral infection are not completely clarified. In this study, we found that the efficacy of Ad infection into CD14+ monocytes was significantly decreased after CD3+ T lymphocytes depletion from PBMC samples of Ad-seropositive individuals. In contrast, adding virus-specific CD3+ T lymphocytes into PBMC samples of Ad-seronegative individuals resulted in a significant increase of infection efficacy. CD3+ T lymphocytes in PBMC samples from Ad-seropositive individuals were more sensitive to be activated by adenovirus stimulus, characterized by upregulation of multiple cytokines and activation markers and also enhancement of cell proliferation. Further studies demonstrated that GM-CSF and IL-4 can promote Ad infection by up-regulating the expression of scavenger receptor 1 (SR-A) and integrins αVβ5 receptor of CD14+ cells. And taken together, these results suggest a novel role of virus-specific T cells in mediating enhancement of viral infection, and provide insights to understand the pathogenesis and complicated interactions between viruses and host immune cells.

scholarly journals Innate immune deficiencies are associated with severity and poor prognosis in patients with COVID-19

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Marine Peyneau ◽  
Vanessa Granger ◽  
Paul-Henri Wicky ◽  
Dounia Khelifi-Touhami ◽  
Jean-François Timsit ◽  
...  
Keyword(s):  
Distress Syndrome ◽  
Innate Immune ◽  
Activation Markers ◽  
Extracellular Traps ◽  
Hla Dr ◽  
Immune Deficiencies ◽  
Severe Infections ◽  
Monocyte Subpopulations ◽  
Critical Patients

AbstractCOVID-19 can cause acute respiratory distress syndrome, leading to death in many individuals. Evidence of a deleterious role of the innate immune system is accumulating, but the precise mechanisms involved remain unclear. In this study, we investigated the links between circulating innate phagocytes and severity in COVID-19 patients. We performed in-depth phenotyping of neutrophil and monocyte subpopulations and measured soluble activation markers in plasma. Additionally, anti-microbial functions (phagocytosis, oxidative burst, and NETosis) were evaluated on fresh cells from patients. Neutrophils and monocytes had a strikingly disturbed phenotype, and elevated concentrations of activation markers (calprotectin, myeloperoxidase, and neutrophil extracellular traps) were measured in plasma. Critical patients had increased CD13low immature neutrophils, LOX-1 + and CCR5 + immunosuppressive neutrophils, and HLA-DRlow downregulated monocytes. Markers of immature and immunosuppressive neutrophils were strongly associated with severity. Moreover, neutrophils and monocytes of critical patients had impaired antimicrobial functions, which correlated with organ dysfunction, severe infections, and mortality. Together, our results strongly argue in favor of a pivotal role of innate immunity in COVID-19 severe infections and pleads for targeted therapeutic options.

scholarly journals Innate immune deficiencies in patients with COVID-19

2021 ◽  
Author(s):  
Marine Peyneau ◽  
Vanessa Granger ◽  
Paul-Henri Wicky ◽  
Dounia Khelifi-Touhami ◽  
Jean-François Timsit ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Myeloid Cell ◽  
Innate Immune ◽  
Activation Markers ◽  
Icu Patients ◽  
Cell Functions ◽  
Hla Dr ◽  
Immune Deficiencies ◽  
Severe Infections

AbstractCOVID-19 can cause acute respiratory distress syndrome (ARDS), leading to death in a significant number of individuals. Evidence of a strong role of the innate immune system is accumulating, but the precise cells and mechanism involved remain unclear. In this study, we investigated the links between circulating innate phagocyte phenotype and functions and severity in COVID-19 patients. Eighty-four consecutive patients were included, 44 of which were in intensive care units (ICU). We performed an in-depth phenotyping of neutrophil and monocyte subpopulations and measured soluble activation markers in plasma. Additionally, myeloid cell functions (phagocytosis, oxidative burst, and NETosis) were evaluated on fresh cells from patients. Resulting parameters were linked to disease severity and prognosis. Both ICU and non-ICU patients had circulating neutrophils and monocytes with an activated phenotype, as well as elevated concentrations of soluble activation markers (calprotectin, myeloperoxidase, neutrophil extracellular traps, MMP9, sCD14) in their plasma. ICU patients were characterized by increased CD10low CD13low immature neutrophils, LOX-1+ and CCR5+ immunosuppressive neutrophils, and HLA-DRlow CD14low downregulated monocytes. Markers of immature and immunosuppressive neutrophils were strongly associated with severity and poor outcome. Moreover, neutrophils and monocytes of ICU patients had impaired antimicrobial functions, which correlated with organ dysfunction, severe infections, and mortality. Our study reveals a marked dysregulation of innate immunity in COVID-19 patients, which was correlated with severity and prognosis. Together, our results strongly argue in favor of a pivotal role of innate immunity in COVID-19 severe infections and pleads for targeted therapeutic options.One Sentence SummaryOur study reveals a marked dysregulation of innate immunity in COVID-19 patients, which correlates with severity and prognosis.

Monocyte activation markers during cardiopulmonary bypass

Perfusion ◽  
2003 ◽  
Vol 18 (2) ◽  
pp. 83-86 ◽  
Author(s):  
R Fink ◽  
M Al-Obaidi ◽  
S Grewal ◽  
M Winter ◽  
J Pepper
Keyword(s):  
Cardiac Surgery ◽  
Cardiopulmonary Bypass ◽  
Coronary Sinus ◽  
Renal Tissue ◽  
Monocyte Count ◽  
Activation Markers ◽  
Hla Dr ◽  
Atherosclerotic Process ◽  
Extracorporeal Support

Extracorporeal support during cardiac surgery initiates an inflammatory response, causing damage to cardiac, pulmonary and renal tissue [Post Pump Syndrome (PPS)]. This is accompanied by a neutrophil leucocytosis and lymphopenia, but less is known about the role of monocytes and markers of monocyte activity. We studied 19 patients undergoing cardiac surgery, obtaining blood samples from the aortic root (AR) and from the coronary sinus (< s) before the cardiopulmonary bypass (CPB), 1 min after release of the aortic crossclamp and 10 min after weaning from CPB (periods 1, 2 and 3). Leucocyte count, monocyte count and HLADR, CD15, CD11b and CD62L activation markers were measured. In samples obtained from the coronary sinus (CS), HLA-DR, expressed as a percentage of the monocyte count, decreased between periods 1, 2 and 3 by 78%, 66% and 43%, respectively. A similar change was observed in samples from the AR. Conversely, CD62L increased in the CS samples (55%, 68% and 73%), but revealed a lesser increase in the AR samples (51%, 68% and 63%). The other markers showed little change throughout the procedure. Reduced immunological competence could result from the decrease in HLA-DR counts. Increases in CD62L sensitizes monocytes to the tethering effects of endothelial integrins and might contribute to the atherosclerotic process.

scholarly journals Activated but impaired IFN-γ production of mucosal-associated invariant T cells in patients with hepatocellular carcinoma

2021 ◽  
Vol 9 (11) ◽  
pp. e003685
Author(s):  
Wenyong Huang ◽  
Dongmei Ye ◽  
Wenjing He ◽  
Xiaoshun He ◽  
Xiaomin Shi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
T Cells ◽  
Peripheral Blood ◽  
Healthy Controls ◽  
Activation Markers ◽  
Mait Cells ◽  
Hla Dr ◽  
Ifn Γ ◽  
And Function

ObjectiveMucosal-associated invariant T (MAIT) cells are innate T cells with immunoregulatory activity and were recently found to be associated with various tumor types. The role of intrasinusoidal MAIT cells in hepatocellular carcinoma (HCC) has not been fully characterized.DesignPeripheral blood samples were obtained from patients with HCC and healthy controls. Liver-associated mononuclear cells (LMCs) were collected from liver perfusions of donors and patients with HCC undergoing liver transplantation. Blood and liver perfusates from patients with HCC were analyzed by flow cytometry for CD3 +CD161+Vα7.2+MAIT cell frequency, phenotype, and function.ResultsThere were fewer MAIT cells in the peripheral blood and liver of patients with HCC than in the healthy controls. Interferon-γ (IFN-γ) production by these cells was also reduced. Peripheral MAIT cells showed upregulation of HLA-DR (Human Leukocyte Antigen DR） and the inhibitory molecule PD-1 (Programmed Cell Death Protein 1), but no significant differences in upregulation were found in intrasinusoidal MAIT cells. MAIT cells were significantly enriched in the liver relative to that in the peripheral blood of patients with HCC. High levels of activation markers and exhaustion markers including HLA-DR, CD69, and PD-1 were observed in LMCs of patients with HCC but not in the peripheral blood. Single-cell RNA sequencing revealed that intrasinusoidal MAIT cells exhibited distinct features in patients with HCC and the controls.ConclusionOur study showed that alterations in MAIT cells are associated with HCC. The distinct activity and function of MAIT cells in the peripheral blood and liver of patients with HCC might suggest a potential role of these cells in disease pathogenesis.

scholarly journals The Role of Interleukin-33 in Head and Neck Squamous Cell Carcinoma Is Determined by Its Cellular Sources in the Tumor Microenvironment

2021 ◽  
Vol 10 ◽  
Author(s):  
Liang Peng ◽  
Wei Sun ◽  
Lin Chen ◽  
Wei-Ping Wen
Keyword(s):  
Squamous Cell Carcinoma ◽  
Tumor Microenvironment ◽  
Immune Responses ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Tumor Cells ◽  
Squamous Cell ◽  
Rna Seq ◽  
Interleukin 33

ObjectivesTo investigate the role of interleukin-33 (IL-33) in head and neck squamous cell carcinoma (HNSCC).Materials and MethodsRNA-seq data of 520 cases of HNSCC were retrieved from The Cancer Genome Atlas. The tumor microenvironment was deconstructed by xCell using bulk RNA-seq data. The cohort was dichotomized by the median IL-33 expression level. Immune cell components and molecular markers were compared between the high and low IL-33 groups. The prognostic value of IL-33 was evaluated by the log-rank test. Differential gene expression analysis and KEGG pathway enrichment analysis were also conducted. The relationship between the IL-33 expression level and the abundance of its potential cellular sources was evaluated by Pearson’s partial correlation test. Subgroup analysis was conducted in laryngeal, oropharyngeal, and oral cavity squamous cell carcinoma (LSCC, OPSCC, and OCSCC).ResultsThe role of IL-33 in HNSCC was heterogeneous among tumors at different sites. In LSCC, IL-33 may increase the extent of malignancy of tumor cells and act as a pro-tumor factor. In OCSCC, IL-33 may play a role in orchestrating the immune responses against tumor cells and act as an antitumor factor. The role of IL-33 in OPSCC was undetermined. IL-33 in LSCC was mainly derived from endothelial cells, while IL-33 in OCSCC was mainly derived from endothelial and epithelial cells.ConclusionAccording to the different sources of IL-33 in LSCC and OCSCC, we propose a hypothesis that stroma-derived IL-33 could favor tumor progression, while epithelial-derived IL-33 could favor antitumor immune responses in HNSCC.

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