scholarly journals Sexual dimorphism in an animal model of Sjo gren's syndrome: a potential role for Th17 cells

Biology Open ◽  
2015 ◽  
Vol 4 (11) ◽  
pp. 1410-1419 ◽  
Author(s):  
A. Voigt ◽  
L. Esfandiary ◽  
C. Q. Nguyen
Keyword(s):  
Animal Model ◽  
Sexual Dimorphism ◽  
Th17 Cells ◽  
Potential Role

scholarly journals Adipose Tissue Immunomodulation and Treg/Th17 Imbalance in the Impaired Glucose Metabolism of Children with Obesity

Children ◽  
2021 ◽  
Vol 8 (7) ◽  
pp. 554
Author(s):  
Stefania Croce ◽  
Maria Antonietta Avanzini ◽  
Corrado Regalbuto ◽  
Erika Cordaro ◽  
Federica Vinci ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Th17 Cells ◽  
Metabolic Disorders ◽  
Potential Role ◽  
Immune Monitoring ◽  
Metabolic Dysfunction ◽  
Impaired Glucose Metabolism ◽  
T Cell Infiltration

In the last few decades, obesity has increased dramatically in pediatric patients. Obesity is a chronic disease correlated with systemic inflammation, characterized by the presence of CD4 and CD8 T cell infiltration and modified immune response, which contributes to the development of obesity related diseases and metabolic disorders, including impaired glucose metabolism. In particular, Treg and Th17 cells are dynamically balanced under healthy conditions, but imbalance occurs in inflammatory and pathological states, such as obesity. Some studies demonstrated that peripheral Treg and Th17 cells exhibit increased imbalance with worsening of glucose metabolic dysfunction, already in children with obesity. In this review, we considered the role of adipose tissue immunomodulation and the potential role played by Treg/T17 imbalance on the impaired glucose metabolism in pediatric obesity. In the patient care, immune monitoring could play an important role to define preventive strategies of pediatric metabolic disease treatments.

scholarly journals Potential role of the antimicrobial peptide Tachyplesin III against multidrug-resistant P. aeruginosa and A. baumannii coinfection in an animal model

2019 ◽  
Vol Volume 12 ◽  
pp. 2865-2874 ◽  
Author(s):  
Jialong Qi ◽  
Ruiyu Gao ◽  
Cunbao Liu ◽  
Bin Shan ◽  
Fulan Gao ◽  
...  
Keyword(s):  
Animal Model ◽  
Antimicrobial Peptide ◽  
Potential Role ◽  
Multidrug Resistant

scholarly journals Potential role of α-synuclein in neurodegeneration: studies in a rat animal model

2012 ◽  
Vol 122 (4) ◽  
pp. 812-822 ◽  
Author(s):  
George Stoica ◽  
Gina Lungu ◽  
Nicole L. Bjorklund ◽  
Giulio Taglialatela ◽  
Xing Zhang ◽  
...  
Keyword(s):  
Animal Model ◽  
Potential Role ◽  
Rat Animal Model

scholarly journals Prolactin in multiple sclerosis

2012 ◽  
Vol 19 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Simon Zhornitsky ◽  
V Wee Yong ◽  
Samuel Weiss ◽  
Luanne M Metz
Keyword(s):  
Multiple Sclerosis ◽  
Systematic Review ◽  
Animal Model ◽  
Optic Neuritis ◽  
Potential Role ◽  
Systematic Search ◽  
Clinical Relapse ◽  
Inclusion Criteria ◽  
Hypothalamic Lesions ◽  
The Impact

Multiple sclerosis (MS) is more common among women than men. MS often goes into remission during pregnancy, when prolactin (PRL) levels are known to be high. In an animal model of demyelination, PRL promoted myelin repair, suggesting it has potential as a remyelinating therapy in MS. In this systematic review, we examined the known associations between PRL and MS, in order to elucidate its potential role in the pathophysiology and treatment of MS. A systematic search was performed in the electronic databases PubMed and EMBASE, using the keywords "prolactin" AND “multiple sclerosis.” The inclusion criteria were met by 23 studies. These studies suggested to us that elevated PRL may be more common in MS patients than in controls. Hyperprolactinemia may also be associated with clinical relapse in MS, especially among patients with hypothalamic lesions or optic neuritis; however, it is unknown if this is a cause or consequence of a relapse. Overall, most people with MS have normal PRL levels. The impact of PRL on MS outcomes remains unclear.

scholarly journals High Resolution Mass Cytometry (CyTOF) in Aplastic Anaemia (AA) Can Identify an Aberrant Treg Subset with Pro-Inflammatory Properties, Predicting Poor Response to Immunosuppressive Therapy

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 1600-1600 ◽  
Author(s):  
Shahram Kordasti ◽  
Thomas Seidl ◽  
Richard J Ellis ◽  
Austin Kulasekararaj ◽  
Xingmin Feng ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
High Resolution ◽  
Immunosuppressive Therapy ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Potential Role ◽  
Mass Cytometry ◽  
Intracellular Staining ◽  
Treg Subset ◽  
Pre Treatment

Abstract Introduction Immune mediated self-response is an established feature of aplastic anaemia (AA) and up to 70% of patients respond to immunosuppressive therapy (IST). Reduced number and function of Tregs and an increase in Th17 cells, similar to other autoimmune conditions, have been reported in AA. Nevertheless, the potential role of these cells in response to IST is not fully understood. Our understanding of human Tregs and Th17 cells and their plasticity has been greatly improved by discovery of phenotypically and functionally distinct subsets. However, due to low number of such cells and technical difficulties for multicolour staining, it is challenging to investigate these subsets in AA and their potential role in response to IST. Mass cytometry (as implemented in the Fluidigm CyTOF instrument) is a technology which allows functional phenotypying of currently up to 40 parameters on a single cell level. In contrast to conventional polychromatic flow cytometry, where the overlap of fluorochrome emission spectra limit the maximum number of 12-14 markers, mass cytometry uses metal isotope-conjugated antibodies to enable "deep immune profiling". We have designed mass cytometry panels for both cell surface and intracellular antigens and used the CyTOF instrument to acquire immune signatures of peripheral blood (PB) samples of AA patients. Patients and Methods Peripheral blood samples from 9 AA patients (7 responders to IST, 2 non-responsers) and 2 healthy donors were collected at diagnosis and following treatment with rabbit or horse ATG and ciclosporin. PBMCs were rested overnight and stained (surface and intracellular) without and with 4 hours stimulation with Phorbol 12-myristate 13-acetate (PMA)/ ionomycin. We designed and optimised 2 separate panels of antibodies based on 41 surface markers, transcription factors and cytokines (table 1). Each antibody is tagged with a unique lanthanide isotope. Acquired data were analysed as .fcs files by both conventional gating and multidimensional Spanning tree Progression of Density normalized Events (SPADE) clustering. Results Viable Lymphocytes were identified by gating on cell length, DNA content, Rh viability dye and CD45 expression. Tregs were then clustered based on CD3, CD4, CD25, CD27, CD127, CD45RA, CD45RO, CD62L and FOXP3. Treg subset II (as defined by Sakaguchi, et al) was identified within total Tregs, based on CD45RA_lo, CD127_lo and FOXP3_hi. The relative expression of all the other markers on Treg II cluster was then calculated based on median values and scale cofactor. AA Tregs at diagnosis expressed significantly higher CD45RA (p<0.001), CD127 (p<0.001), CD7 (p=0.04), CD69 (p=0.03), CD103 (p=0.02), T-bet (p=0.01), and IL-4 (p=0.008) compared to HD, whereas the expression of CD152 (CTLA-4) and HLA-DR were significantly lower in AA (p=0.04 and p=0.03). When patients were grouped as responders and non-responders to IST, Tregs from non-responders patients expressed significantly higher CD11b (p=0.04), CD45RA (p<0.001), CD127 (p<0.001), CCR4 (p=0.02), IL-2 (p=0.03), IL-4 (p=0.02), IL-6 (p=0.04), T-bet (p=0.008), IL-17 (p=0.01) and GATA3 (p<0.001) while the expression of FOXP3 (p=0.03), CD7 (p=0.01) and CD25 (p=0.03) was lower compared to responders. Following IST the expression of CD45RA, CD7 and IL-4 by Tregs were reduced (p=0.004, p<0.001 and p=0.02) whereas CD152 increased (p<0.01) compared to pre-treatment Tregs. When Treg cytokine profiles following response to IST were compared to pre-treatment Tregs from non responder patients, we have noticed a significantly lower secretion of other pro-inflammatory cytokines including IL-6 (p=0.01) and IL-17 (p=0.03) as well as IL-2 (p=0.03) by post IST Tregs. These Tregs were also less T-bet positive (p=0.02)(figures 1 and 2). Conclusions We demonstrate the ability of mass cytometry to define in high resolution the immunophenotypes of very specific subsets of Tregs in AA that is extremely challenging by conventional flow-cytometry. Our data indicate that a combination of pro-inflammatory and activation markers defines a subset of Tregs, which could potentially predict response to IST. Similar studies in a larger cohort of patients should delineate a more specific immune signature for the evaluation of response and follow up of AA patients following non-transplant treatments. Table1: Markers for surface and intracellular staining. Table1:. Markers for surface and intracellular staining. Disclosures No relevant conflicts of interest to declare.

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