Immunological characteristics of acute urogenital monochlamydiosis

1999 ◽  
Vol 48 (4) ◽  
pp. 21-25
Author(s):  
O. G. Bugrova ◽  
E. F. Kira ◽  
A. M. Savitcheva
Keyword(s):  
Immune Cells ◽  
Receptor Expression ◽  
Functional Potential

The article stresses that the use of two modem methods: luminescent and lactincytochemical has helped to understand the receptor expression for bionic amines, catecholamines and pectines, that depicts the functional potential of mucous and immune cells in urogenital chlamydiosis.

Muscarinic acetylcholine receptor expression in brain and immune cells of Oreochromis niloticus

2019 ◽  
Vol 328 ◽  
pp. 105-107 ◽  
Author(s):  
C.E. Covantes-Rosales ◽  
G.A. Toledo-Ibarra ◽  
K.J.G. Díaz-Resendíz ◽  
G.H. Ventura-Ramón ◽  
M.I. Girón-Pérez
Keyword(s):  
Acetylcholine Receptor ◽  
Immune Cells ◽  
Oreochromis Niloticus ◽  
Muscarinic Acetylcholine Receptor ◽  
Receptor Expression ◽  
Muscarinic Acetylcholine

CCR2 knockout exacerbates cerulein-induced chronic pancreatitis with hyperglycemia via decreased GLP-1 receptor expression and insulin secretion

2013 ◽  
Vol 304 (8) ◽  
pp. G700-G707 ◽  
Author(s):  
Yuji Nakamura ◽  
Takanori Kanai ◽  
Keita Saeki ◽  
Miho Takabe ◽  
Junichiro Irie ◽  
...  
Keyword(s):  
Cell Migration ◽  
Insulin Secretion ◽  
Chronic Pancreatitis ◽  
Immune Cells ◽  
Receptor Expression ◽  
Wild Type ◽  
Multiple Series ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Relationship

Glucagon-like peptide-1 (GLP-1) promotes insulin release; however, the relationship between the GLP-1 signal and chronic pancreatitis is not well understood. Here we focus on chemokine (C-C motif) ligand 2 (CCL2) and its receptor (CCR2) axis, which regulates various immune cells, including macrophages, to clarify the mechanism of GLP-1-mediated insulin secretion in chronic pancreatitis in mice. One and multiple series of repetitive cerulein administrations were used to induce acute and chronic cerulein pancreatitis, respectively. Acute cerulein-administered CCR2-knockout (KO) mice showed suppressed infiltration of CD11b+Gr-1low macrophages and pancreatic inflammation and significantly upregulated insulin secretion compared with paired wild-type (WT) mice. However, chronic cerulein-administered CCR2-KO mice showed significantly increased infiltration of CD11b+/Gr-1− and CD11b+/Gr-1high cells, but not CD11b+/Gr-1low cells, in pancreas with severe inflammation and significantly decreased insulin secretion compared with their WT counterparts. Furthermore, although serum GLP-1 levels in chronic cerulein-administered WT and CCR2-KO mice were comparably upregulated after cerulein administrations, GLP-1 receptor levels in pancreases of chronic cerulein-administered CCR2-KO mice were significantly lower than in paired WT mice. Nevertheless, a significantly higher hyperglycemia level in chronic cerulein-administered CCR2-KO mice was markedly restored by treatment with a GLP-1 analog to a level comparable to the paired WT mice. Collectively, the CCR2/CCL2 axis-mediated CD11b+-cell migration to the pancreas is critically involved in chronic pancreatitis-mediated hyperglycemia through the modulation of GLP-1 receptor expression and insulin secretion.

scholarly journals Opioids and clonidine modulate cytokine production and opioid receptor expression in neonatal immune cells

2012 ◽  
Vol 33 (5) ◽  
pp. 374-382 ◽  
Author(s):  
R Chavez-Valdez ◽  
L Kovell ◽  
R Ahlawat ◽  
G L McLemore ◽  
M Wills-Karp ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Immune Cells ◽  
Cytokine Production ◽  
Receptor Expression

HIV-1 co-receptor expression and epithelial immune cells of the cervix in asymptomatic women attending a genitourinary medicine clinic

HIV Medicine ◽  
2012 ◽  
Vol 14 (2) ◽  
pp. 108-114 ◽  
Author(s):  
CP McClure ◽  
CA Bowman ◽  
I Geary ◽  
C Ryan ◽  
JK Ball ◽  
...  
Keyword(s):  
Immune Cells ◽  
Receptor Expression ◽  
Medicine Clinic ◽  
Genitourinary Medicine ◽  
Asymptomatic Women ◽  
Hiv 1

Tumour-mediated TRAIL-receptor Expression Indicates Effective Apoptotic Depletion of Infiltrating CD8+ Immune Cells in Clinical Colorectal Cancer

2010 ◽  
Vol 135 ◽  
pp. S60-S61
Author(s):  
Martin Gasser ◽  
Martin Grimm ◽  
Mia Kim ◽  
Andreas Rosenwald ◽  
Christoph Germer ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Immune Cells ◽  
Receptor Expression ◽  
Trail Receptor

scholarly journals Therapeutic melanoma inhibition by local micelle-mediated cyclic nucleotide repression

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Kerstin Johann ◽  
Toszka Bohn ◽  
Fatemeh Shahneh ◽  
Natascha Luther ◽  
Alexander Birke ◽  
...  
Keyword(s):  
Immune Cells ◽  
Antitumor Immunity ◽  
Immune Escape ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Benzyl Ester ◽  
Receptor Expression ◽  
Single Cell Sequencing ◽  
Copolymer Micelles ◽  
Toxic Concentrations

AbstractThe acidic tumor microenvironment in melanoma drives immune evasion by up-regulating cyclic adenosine monophosphate (cAMP) in tumor-infiltrating monocytes. Here we show that the release of non-toxic concentrations of an adenylate cyclase (AC) inhibitor from poly(sarcosine)-block-poly(L-glutamic acid γ-benzyl ester) (polypept(o)id) copolymer micelles restores antitumor immunity. In combination with selective, non-therapeutic regulatory T cell depletion, AC inhibitor micelles achieve a complete remission of established B16-F10-OVA tumors. Single-cell sequencing of melanoma-infiltrating immune cells shows that AC inhibitor micelles reduce the number of anti-inflammatory myeloid cells and checkpoint receptor expression on T cells. AC inhibitor micelles thus represent an immunotherapeutic measure to counteract melanoma immune escape.

scholarly journals Hyperinflammatory environment drives dysfunctional myeloid cell effector response to bacterial challenge in COVID-19

2022 ◽  
Vol 18 (1) ◽  
pp. e1010176
Author(s):  
Srikanth Mairpady Shambat ◽  
Alejandro Gómez-Mejia ◽  
Tiziano A. Schweizer ◽  
Markus Huemer ◽  
Chun-Chi Chang ◽  
...  
Keyword(s):  
Acute Phase ◽  
Immune Cells ◽  
Bacterial Infections ◽  
Receptor Expression ◽  
Cell Surface Receptor ◽  
High Expression ◽  
Cytokine Signaling ◽  
Bacterial Challenge ◽  
Functional Responses ◽  
Low Expression

COVID-19 displays diverse disease severities and symptoms including acute systemic inflammation and hypercytokinemia, with subsequent dysregulation of immune cells. Bacterial superinfections in COVID-19 can further complicate the disease course and are associated with increased mortality. However, there is limited understanding of how SARS-CoV-2 pathogenesis and hypercytokinemia impede the innate immune function against bacterial superinfections. We assessed the influence of COVID-19 plasma hypercytokinemia on the functional responses of myeloid immune cells upon bacterial challenges from acute-phase COVID-19 patients and their corresponding recovery (rec)-phase. We show that a severe hypercytokinemia status in COVID-19 patients correlates with the development of bacterial superinfections. Neutrophils and monocytes derived from COVID-19 patients in their acute-phase showed an impaired intracellular microbicidal capacity upon bacterial challenges. The impaired microbicidal capacity was reflected by abrogated MPO and reduced NETs production in neutrophils along with reduced ROS production in both neutrophils and monocytes. Moreover, we observed a distinct pattern of cell surface receptor expression on both neutrophils and monocytes, in line with suppressed autocrine and paracrine cytokine signaling. This phenotype was characterized by a high expression of CD66b, CXCR4 and low expression of CXCR1, CXCR2 and CD15 in neutrophils and low expression of HLA-DR, CD86 and high expression of CD163 and CD11b in monocytes. Furthermore, the impaired antibacterial effector function was mediated by synergistic effect of the cytokines TNF-α, IFN-γ and IL-4. COVID-19 patients receiving dexamethasone showed a significant reduction of overall inflammatory markers in the plasma as well as exhibited an enhanced immune response towards bacterial challenge ex vivo. Finally, broad anti-inflammatory treatment was associated with a reduction in CRP, IL-6 levels as well as length of ICU and hospital stay in critically ill COVID-19 patients. Our data provides insights into the transient functional dysregulation of myeloid immune cells against subsequent bacterial infections in COVID-19 patients and describe a beneficial role for the use of dexamethasone in these patients.

scholarly journals Contribution of Immune Cells to Glucocorticoid Receptor Expression in Breast Cancer

2020 ◽  
Vol 21 (13) ◽  
pp. 4635 ◽  
Author(s):  
Shipra Gandhi ◽  
Ahmed Elkhanany ◽  
Masanori Oshi ◽  
Tao Dai ◽  
Mateusz Opyrchal ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucocorticoid Receptor ◽  
Single Cell ◽  
Immune Cells ◽  
Receptor Expression ◽  
Gene Set Enrichment Analysis ◽  
Proliferation Index ◽  
Sequencing Data ◽  
Single Cell Sequencing ◽  
Risk Of Cancer

Breast cancer (BC) patients experience increased stress with elevated cortisol levels, increasing risk of cancer recurrence. Cortisol binds to a cytoplasmic receptor, glucocorticoid receptor (GR) encoded by GR gene (NR3C1). We hypothesized that not only cancer cells, but even immune cells in the tumor microenvironment (TME) may contribute to GR expression in bulk tumor and influence prognosis. To test this, mRNA expression data was accessed from METABRIC and TCGA. “High” and “low” expression was based on highest and lowest quartiles of NR3C1 gene expression, respectively. Single-cell sequencing data were obtained from GSE75688 and GSE114725 cohorts. Computer algorithms CIBERSORT, Gene Set Enrichment Analysis and TIMER were used. GR-high BC has better median disease-free and disease-specific survival. Single cell sequencing data showed higher GR expression on immune cells compared to cancer and stromal cells. Positive correlation between GR-high BC and CD8+ T-cells was noted. In GR-high tumors, higher cytolytic activity (CYT) with decreased T-regulatory and T-follicular helper cells was observed. High GR expression was associated with lower proliferation index Ki67, enriched in IL-2_STAT5, apoptosis, KRAS, TGF-β signaling, and epithelial-to-mesenchymal transition. Immune cells significantly contribute to GR expression of bulk BC. GR-high BC has a favorable TME with higher CYT with favorable outcomes.

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