scholarly journals The Role of NF-κB in Uterine Spiral Arteries Remodeling, Insight into the Cornerstone of Preeclampsia

2021 ◽  
Vol 22 (2) ◽  
pp. 704
Author(s):  
Maciej W. Socha ◽  
Bartosz Malinowski ◽  
Oskar Puk ◽  
Mateusz Wartęga ◽  
Martyna Stankiewicz ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Gestational Hypertension ◽  
Therapeutic Option ◽  
Risk Groups ◽  
Selective Inhibition ◽  
Cell Phenotype ◽  
Maternal Circulation ◽  
Uterine Natural Killer Cells ◽  
Promising Therapeutic Target ◽  
And Function

Preeclampsia is one of the three leading causes of maternal morbidity and mortality worldwide. It afflicts 2–8% of pregnancies and is the most common cause of gestational hypertension. This article is focused on nuclear factor kappa B (NF-κB), its role in normal and pathological spiral arteries remodelling and development of preeclampsia, with evaluation if it is a promising therapeutic target. NF-κB is a key mediator of placentation. Since insemination, it stimulates production of proinflammatory cytokines by the uterine epithelium, which leads to activation of macrophages, uterine natural killer cells (uNKs), and other leukocytes. The trophoblast/uNK/macrophage crosstalk is crucial for implantation and spiral arteries remodeling, and NF-κB regulates that process through modification of cytokine expression, as well as cell phenotype and function. In the course of preeclampsia, the remodeling processes is disturbed by excessive inflammation and increased NF-κB activation. The pathological remodeling leads to uteroplacental dysfunction, release of proinflammatory cytokines into the maternal circulation, endothelial stress, and development of preeclampsia. The analysis of genetic and environmental inductors of NF-κB helps to distinguish preeclampsia risk groups. Furthermore, a selective inhibition of NF-κB or NF-κB activating pathways alleviates symptoms of preeclampsia in rat models; therefore, this could be an efficient therapeutic option.

scholarly journals Impacts of HIV infection on Vγ2Vδ2 T cell phenotype and function: a mechanism for reduced tumor immunity in AIDS

2008 ◽  
Vol 84 (2) ◽  
pp. 371-379 ◽  
Author(s):  
Jean-Saville Cummings ◽  
Cristiana Cairo ◽  
Cheryl Armstrong ◽  
Charles E. Davis ◽  
C. David Pauza
Keyword(s):  
T Cell ◽  
Hiv Infection ◽  
Tumor Immunity ◽  
Cell Phenotype ◽  
And Function

scholarly journals Pathophysiology of acute respiratory syndrome coronavirus 2 infection: a systematic literature review to inform EULAR points to consider

RMD Open ◽  
2021 ◽  
Vol 7 (1) ◽  
pp. e001549 ◽  
Author(s):  
Aurélie Najm ◽  
Alessia Alunno ◽  
Xavier Mariette ◽  
Benjamin Terrier ◽  
Gabriele De Marco ◽  
...  
Keyword(s):  
Literature Review ◽  
Systematic Literature Review ◽  
Immune Cell ◽  
Severe Disease ◽  
Cell Phenotype ◽  
Loss Of Function ◽  
Humoral And Cellular Immunity ◽  
Host Immune Responses ◽  
Disease Spectrum ◽  
And Function

BackgroundThe SARS-CoV-2 pandemic is a global health problem. Beside the specific pathogenic effect of SARS-CoV-2, incompletely understood deleterious and aberrant host immune responses play critical roles in severe disease. Our objective was to summarise the available information on the pathophysiology of COVID-19.MethodsTwo reviewers independently identified eligible studies according to the following PICO framework: P (population): patients with SARS-CoV-2 infection; I (intervention): any intervention/no intervention; C (comparator): any comparator; O (outcome) any clinical or serological outcome including but not limited to immune cell phenotype and function and serum cytokine concentration.ResultsOf the 55 496 records yielded, 84 articles were eligible for inclusion according to question-specific research criteria. Proinflammatory cytokine expression, including interleukin-6 (IL-6), was increased, especially in severe COVID-19, although not as high as other states with severe systemic inflammation. The myeloid and lymphoid compartments were differentially affected by SARS-CoV-2 infection depending on disease phenotype. Failure to maintain high interferon (IFN) levels was characteristic of severe forms of COVID-19 and could be related to loss-of-function mutations in the IFN pathway and/or the presence of anti-IFN antibodies. Antibody response to SARS-CoV-2 infection showed a high variability across individuals and disease spectrum. Multiparametric algorithms showed variable diagnostic performances in predicting survival, hospitalisation, disease progression or severity, and mortality.ConclusionsSARS-CoV-2 infection affects both humoral and cellular immunity depending on both disease severity and individual parameters. This systematic literature review informed the EULAR ‘points to consider’ on COVID-19 pathophysiology and immunomodulatory therapies.

miR‐223 promotes regenerative myeloid cell phenotype and function in the demyelinated central nervous system

Glia ◽  
2018 ◽  
Vol 67 (5) ◽  
pp. 857-869 ◽  
Author(s):  
Dylan A. Galloway ◽  
Stephanie N. Blandford ◽  
Tangyne Berry ◽  
John B. Williams ◽  
Mark Stefanelli ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Myeloid Cell ◽  
Cell Phenotype ◽  
And Function

scholarly journals Cytometric analysis of cell phenotype and function

Leukemia ◽  
2002 ◽  
Vol 16 (12) ◽  
pp. 2463-2464
Author(s):  
MRG O'Gorman
Keyword(s):  
Cell Phenotype ◽  
And Function

scholarly journals Sex differences in autoimmunity could be associated with altered regulatory T cell phenotype and lipoprotein metabolism

2019 ◽  
Author(s):  
George A Robinson ◽  
Kirsty E Waddington ◽  
Marsilio Adriani ◽  
Anna Radziszewska ◽  
Hannah Peckham ◽  
...  
Keyword(s):  
Sex Differences ◽  
T Cell ◽  
Regulatory T Cell ◽  
Immune Cell ◽  
Pubertal Development ◽  
Cell Subset ◽  
Cell Phenotype ◽  
Healthy Adolescent ◽  
Treg Frequency ◽  
And Function

ABSTRACTMale and female immune responses are known to differ resulting in an increased prevalence of autoimmunity in women. Here sex differences in T-cell subset frequency and function during adolescence were examined in healthy donors and patients with the autoimmune disease juvenile (J)SLE; onset of JSLE commonly occurs during puberty suggesting a strong hormonal influence. Healthy adolescent males had increased regulatory T-cell (Treg) frequency, and increased Treg suppressive capacity and IL-4 production compared to healthy adolescent females. The T-helper 2-like profile in male Tregs was associated with increased expression of GATA3 which correlated significantly with elevated Treg plasma membrane glycosphingolipid expression. Differential Treg phenotype was associated with unique serum metabolomic profiles in males compared to female adolescents. Notably, very low density lipoprotein (VLDL) metabolomic signatures correlated positively with activated Tregs in males but with resting Tregs in females. Consistently, only VLDL isolated from male serum was able to induce increased Treg IL-4 production and glycosphingolipid expression following in cultured cells. Remarkably, gender differences in Treg frequency, phenotype and function and serum metabolomic profiles were lost in adolescents with JSLE. This work provides evidence that a combination of pubertal development, immune cell defects and dyslipidemia may contribute to JSLE pathogenesis.

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