Reduction in immune cell number and loss of 5hmC are associated with lesion grade in cervical carcinogenesis

3 Biotech ◽  
2021 ◽  
Vol 11 (11) ◽  
Author(s):  
Xiaohan Yang ◽  
Xinyue Shen ◽  
Zhujun Li ◽  
Wencai Li ◽  
Ying Liu
Keyword(s):  
Immune Cell ◽  
Cell Number ◽  
Cervical Carcinogenesis

scholarly journals Cdx2 regulates immune cell infiltration in the intestine

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Simon Chewchuk ◽  
Sanzida Jahan ◽  
David Lohnes
Keyword(s):  
Intestinal Epithelium ◽  
Target Genes ◽  
Immune Cell ◽  
Cell Number ◽  
Macrophage Infiltration ◽  
Intestinal Homeostasis ◽  
Chronic Inflammatory Response ◽  
Complex Protein ◽  
Inflammatory Phenotype

AbstractThe intestinal epithelium is a unique tissue, serving both as a barrier against pathogens and to conduct the end digestion and adsorption of nutrients. As regards the former, the intestinal epithelium contains a diverse repertoire of immune cells, including a variety of resident lymphocytes, macrophages and dendritic cells. These cells serve a number of roles including mitigation of infection and to stimulate regeneration in response to damage. The transcription factor Cdx2, and to a lesser extent Cdx1, plays essential roles in intestinal homeostasis, and acts as a context-dependent tumour suppressor in colorectal cancer. Deletion of Cdx2 from the murine intestinal epithelium leads to macrophage infiltration resulting in a chronic inflammatory response. However the mechanisms by which Cdx2 loss evokes this response are poorly understood. To better understand this relationship, we used a conditional mouse model lacking all intestinal Cdx function to identify potential target genes which may contribute to this inflammatory phenotype. One such candidate encodes the histocompatability complex protein H2-T3, which functions to regulate intestinal iCD8α lymphocyte activity. We found that Cdx2 occupies the H3-T3 promoter in vivo and directly regulates its expression via a Cdx response element. Loss of Cdx function leads to a rapid and pronounced attenuation of H2-T3, followed by a decrease in iCD8α cell number, an increase in macrophage infiltration and activation of pro-inflammatory cascades. These findings suggest a previously unrecognized role for Cdx in intestinal homeostasis through H2-T3-dependent regulation of iCD8α cells.

scholarly journals The impact of leukapheresis on immune-cell number and function in patients with advanced cancer

2015 ◽  
Vol 64 (11) ◽  
pp. 1429-1435 ◽  
Author(s):  
James L. Gulley ◽  
Jennifer Marté ◽  
Christopher R. Heery ◽  
Ravi A. Madan ◽  
Seth M. Steinberg ◽  
...  
Keyword(s):  
Advanced Cancer ◽  
Immune Cell ◽  
Cell Number ◽  
And Function ◽  
The Impact

scholarly journals Chimeric antigen receptors that trigger phagocytosis

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Meghan A Morrissey ◽  
Adam P Williamson ◽  
Adriana M Steinbach ◽  
Edward W Roberts ◽  
Nadja Kern ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Immune Cell ◽  
Human Cancer ◽  
Antibody Fragment ◽  
Cell Number ◽  
Antigen Receptors ◽  
Chimeric Antigen Receptors ◽  
Cell Therapies ◽  
Human Cancer Cells

Chimeric antigen receptors (CARs) are synthetic receptors that reprogram T cells to kill cancer. The success of CAR-T cell therapies highlights the promise of programmed immunity and suggests that applying CAR strategies to other immune cell lineages may be beneficial. Here, we engineered a family of Chimeric Antigen Receptors for Phagocytosis (CAR-Ps) that direct macrophages to engulf specific targets, including cancer cells. CAR-Ps consist of an extracellular antibody fragment, which can be modified to direct CAR-P activity towards specific antigens. By screening a panel of engulfment receptor intracellular domains, we found that the cytosolic domains from Megf10 and FcRɣ robustly triggered engulfment independently of their native extracellular domain. We show that CAR-Ps drive specific engulfment of antigen-coated synthetic particles and whole human cancer cells. Addition of a tandem PI3K recruitment domain increased cancer cell engulfment. Finally, we show that CAR-P expressing murine macrophages reduce cancer cell number in co-culture by over 40%.

scholarly journals TM4SF5-mediated liver malignancy involves NK cell exhaustion-like phenotypes

2021 ◽  
Author(s):  
Hyunseung Sun ◽  
Eunmi Kim ◽  
Jihye Ryu ◽  
Hyejin Lee ◽  
Eun-Ae Shin ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Mouse Models ◽  
Immune Cell ◽  
Nk Cell ◽  
Cell Number ◽  
Liver Carcinogenesis ◽  
Liver Malignancy ◽  
Cell Exhaustion

AbstractAberrant extracellular matrix and immune cell alterations within the tumor microenvironment promote the pathological progression of liver carcinogenesis. Although transmembrane 4 L six family member 5 (TM4SF5) is involved in liver fibrosis and cancer, its mechanism avoiding immune surveillance during carcinogenesis remains unknown. We investigated how TM4SF5-mediated signaling caused immune evasion using in vitro primary cells and in vivo liver tissues from genetic or chemically induced mouse models. TM4SF5-transgenic and diethylnitrosamine (DEN)-induced liver cancer mouse models exhibited fibrotic and cancerous livers, respectively, with enhanced TM4SF5, pY705STAT3, collagen I, and laminin γ2 levels. These TM4SF5-mediated effects were abolished by TM4SF5 inhibitor, 4′-(p-toluenesulfonylamido)-4-hydroxychalcone (TSAHC). TM4SF5-dependent tumorigenesis involved natural killer (NK) cell exhaustion-like phenotypes including the reduction of NK cell number or function, which were blocked with TSAHC treatment. TM4SF5 expression in cancer cells downregulated stimulatory ligands and receptors for NK cell cytotoxicity, including SLAMF6, SLAMF7, MICA/B, and others. TM4SF5 suppression or inhibition reduced STAT3 signaling activity and recovered the receptor levels and NK cell surveillance, leading to reduced fibrotic and cancerous phenotypes, and longer survival. Altogether, these findings suggest that TM4SF5-mediated STAT3 activity for extracellular matrix modulation is involved in the progression of liver disease to HCC and that TM4SF5 appears to suppress NK cells during liver carcinogenesis.

scholarly journals Chemokine Receptor-6 Promotes B-1 Cell Trafficking to Perivascular Adipose Tissue, Local IgM Production and Atheroprotection

2021 ◽  
Vol 12 ◽  
Author(s):  
Prasad Srikakulapu ◽  
Aditi Upadhye ◽  
Fabrizio Drago ◽  
Heather M. Perry ◽  
Sai Vineela Bontha ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
B Cells ◽  
B Cell ◽  
Chemokine Receptor ◽  
Immune Cell ◽  
Cell Number ◽  
Cell Trafficking ◽  
Perivascular Adipose Tissue ◽  
Major Mechanism ◽  
High Level

Chemokine receptor-6 (CCR6) mediates immune cell recruitment to inflammatory sites and has cell type-specific effects on diet-induced atherosclerosis in mice. Previously we showed that loss of CCR6 in B cells resulted in loss of B cell-mediated atheroprotection, although the B cell subtype mediating this effect was unknown. Perivascular adipose tissue (PVAT) harbors high numbers of B cells including atheroprotective IgM secreting B-1 cells. Production of IgM antibodies is a major mechanism whereby B-1 cells limit atherosclerosis development. Yet whether CCR6 regulates B-1 cell number and production of IgM in the PVAT is unknown. In this present study, flow cytometry experiments demonstrated that both B-1 and B-2 cells express CCR6, albeit at a higher frequency in B-2 cells in both humans and mice. Nevertheless, B-2 cell numbers in peritoneal cavity (PerC), spleen, bone marrow and PVAT were no different in ApoE−/−CCR6−/− compared to ApoE−/−CCR6+/+ mice. In contrast, the numbers of atheroprotective IgM secreting B-1 cells were significantly lower in the PVAT of ApoE−/−CCR6−/− compared to ApoE−/−CCR6+/+ mice. Surprisingly, adoptive transfer (AT) of CD43− splenic B cells into B cell-deficient μMT−/−ApoE−/− mice repopulated the PerC with B-1 and B-2 cells and reduced atherosclerosis when transferred into ApoE−/−CCR6+/+sIgM−/− mice only when those cells expressed both CCR6 and sIgM. CCR6 expression on circulating human B cells in subjects with a high level of atherosclerosis in their coronary arteries was lower only in the putative human B-1 cells. These results provide evidence that B-1 cell CCR6 expression enhances B-1 cell number and IgM secretion in PVAT to provide atheroprotection in mice and suggest potential human relevance to our murine findings.

EFFECTS OF PRIOR EXERCISE ON IMMUNE CELL NUMBER AND NKCA: ROLE OF BLOOD GLUCOSE AND CORTISOL

1998 ◽  
Vol 30 (Supplement) ◽  
pp. 174
Author(s):  
L. T. Mackinnon ◽  
V. Gedge ◽  
M. G. Flynn
Keyword(s):  
Blood Glucose ◽  
Immune Cell ◽  
Cell Number ◽  
Prior Exercise

scholarly journals Effects of pegylated G-CSF on immune cell number and function in patients with gynecological malignancies

2010 ◽  
Vol 8 (1) ◽  
pp. 114 ◽  
Author(s):  
Giuseppina Bonanno ◽  
Annabella Procoli ◽  
Andrea Mariotti ◽  
Maria Corallo ◽  
Alessandro Perillo ◽  
...  
Keyword(s):  
Immune Cell ◽  
Cell Number ◽  
Gynecological Malignancies ◽  
And Function

Anabolic androgenic steroids effects on the immune system: a review

2009 ◽  
Vol 4 (1) ◽  
pp. 19-33 ◽  
Author(s):  
Sonya Marshall-Gradisnik ◽  
Rachel Green ◽  
Ekua Brenu ◽  
Robert Weatherby
Keyword(s):  
Immune System ◽  
Immune Cell ◽  
Anabolic Steroids ◽  
Cell Number ◽  
Steroid Nucleus ◽  
Regime Types ◽  
Androgenic Anabolic Steroids ◽  
Differentiation And Proliferation ◽  
Androgenic Steroids ◽  
And Function

AbstractAndrogenic anabolic steroids (AAS) are synthetic derivatives of the male hormone testosterone. AAS are used by athletes and recreational users of all ages to enhance their athletic performance and/or physical appearance. While several adverse effects of AAS abuse have been described, their effect on the immune system has not been clearly elucidated. The literature generally indicates that supraphysiologic doses of AAS with an intact steroid nucleus are immunosuppressive, that is they reduce immune cell number and function. While those with alterations to the steroid nucleus are immunostimulatory as they induce the proliferation of T cells and other immune cells. Specifically, several common AAS have been shown to adversely influence lymphocyte differentiation and proliferation, antibody production, Natural Killer Cytotoxic activity and the production of certain cytokines, thereby altering the immune reaction. These effects may be profound and long lasting depending on the dosing regime, types or combinations of AAS used and the extent and duration of AAS abuse. Nevertheless, the effects of long term use of supraphysiologic doses of AAS on the immune system remain uncertain.

scholarly journals Chimeric antigen receptors that trigger phagocytosis

2018 ◽  
Author(s):  
Meghan A. Morrissey ◽  
Adam P. Williamson ◽  
Adriana M. Steinbach ◽  
Edward W. Roberts ◽  
Nadja Kern ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Immune Cell ◽  
Antibody Fragment ◽  
Cell Number ◽  
Antigen Receptors ◽  
Chimeric Antigen Receptors ◽  
Cell Therapies ◽  
Car T ◽  
Cytosolic Domains

AbstractChimeric antigen receptors (CARs) are synthetic receptors that reprogram T cells to kill cancer. The success of CAR-T cell therapies highlights the promise of programmed immunity, and suggests that applying CAR strategies to other immune cell lineages may be beneficial. Here, we engineered a family of Chimeric Antigen Receptors for Phagocytosis (CAR-Ps) that direct macrophages to engulf specific targets, including cancer cells. CAR-Ps consist of an extracellular antibody fragment, which can be modified to direct CAR-P activity towards specific antigens. By screening a panel of engulfment receptor intracellular domains, we found that the cytosolic domains from Megf10 and FcRγ robustly triggered engulfment independently of their native extracellular domain. We show that CAR-Ps drive specific engulfment of antigen-coated synthetic particles and whole cancer cells. Addition of a tandem PI3K recruitment domain increased cancer cell engulfment. Finally, we show that CAR-P expressing macrophages reduce cancer cell number in co-culture by over 40%.SummaryWe report the first Chimeric Antigen Receptors for Phagocytosis (CAR-Ps) that promote engulfment of antigen-coated particles and cancer cells.

scholarly journals Immune Cells Expansion From Peripheral Blood of Patients of Three Leading Cancers in Vietnam

2021 ◽  
Vol 37 (3) ◽  
Author(s):  
Chu Thi Thao ◽  
Bui Viet Anh ◽  
Nguyen Van Phong ◽  
Nguyen Trung Kien ◽  
Nguyen Dac Tu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Viability ◽  
Cancer Treatment ◽  
Cancer Patients ◽  
Cell Expansion ◽  
Immune Cell ◽  
Nk Cell ◽  
Ex Vivo ◽  
Cell Number ◽  
Gastric Cancer Patients

Immunotherapy recently attracted the high attention of scientists in cancer treatment. However, this therapy is poorly studied and applied in Vietnam. In this report, we present the results of immune cell ex vivo expansion for cancer treatment. After 20-21 days of culture, the average number of CD3+CD8+ cytotoxic T lymphocytes (CTLs) increased by 633.6-fold, equivalent to 3277.5 × 106 cells, and with the cell viability was 96.3%. Among them, the increasing fold of lung, liver and gastric cancer patients were 232.4, 812.4 and 655.6 respectively. Meanwhile, the average number of CD3-CD56+ NK cells increased by 940.3-fold, equivalent to 2659.3 × 106 cells, with the cell viability of 95%. Gastric cancer patients had the highest fold of Natural killer (NK) cell expansion (1644.9 fold) compared to that in lung cancer (695.0 fold) and liver cancer patients (358.3 fold). These results revealed that our method of immune cell expansion met the requirements in the immune cell number for clinical applications in cancer treatment in Vietnam.

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