Microenvironment abnormalities and cytokine network deregulation in lymphomagenesis and progression

2015 ◽  
pp. 34-50
Author(s):  
Clifford Blieden ◽  
Nitin Kumar Agarwal ◽  
Francisco Vega
Keyword(s):  
Cytokine Network

A Pathogenic Cytokine Network Is Associated with Pro-Inflammatory B Cells in Systemic Lupus Erythematosus Patients

2019 ◽  
Author(s):  
Quentin Simon ◽  
Alexis Grasseau ◽  
Marina Boudigou ◽  
Laëtitia Le Pottier ◽  
Bénédicte Rouvière ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
B Cells ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Cytokine Network

The Cytokine Network in HIV Infection

2002 ◽  
Vol 2 (8) ◽  
pp. 677-689 ◽  
Author(s):  
M. Alfano ◽  
G. Poli
Keyword(s):  
Hiv Infection ◽  
Cytokine Network

scholarly journals Deconvolution of monocyte responses in inflammatory bowel disease reveals an IL-1 cytokine network that regulates IL-23 in genetic and acquired IL-10 resistance

Gut ◽  
2020 ◽  
pp. gutjnl-2020-321731
Author(s):  
Dominik Aschenbrenner ◽  
Maria Quaranta ◽  
Soumya Banerjee ◽  
Nicholas Ilott ◽  
Joanneke Jansen ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Personalised Medicine ◽  
Mononuclear Phagocytes ◽  
Cytokine Network ◽  
Peripheral Blood Mononuclear ◽  
Transcriptional Signature ◽  
Inflammatory Monocytes ◽  
Transcriptomic Signature ◽  
Inflammatory Bowel

ObjectiveDysregulated immune responses are the cause of IBDs. Studies in mice and humans suggest a central role of interleukin (IL)-23-producing mononuclear phagocytes in disease pathogenesis. Mechanistic insights into the regulation of IL-23 are prerequisite for selective IL-23 targeting therapies as part of personalised medicine.DesignWe performed transcriptomic analysis to investigate IL-23 expression in human mononuclear phagocytes and peripheral blood mononuclear cells. We investigated the regulation of IL-23 expression and used single-cell RNA sequencing to derive a transcriptomic signature of hyperinflammatory monocytes. Using gene network correlation analysis, we deconvolved this signature into components associated with homeostasis and inflammation in patient biopsy samples.ResultsWe characterised monocyte subsets of healthy individuals and patients with IBD that express IL-23. We identified autosensing and paracrine sensing of IL-1α/IL-1β and IL-10 as key cytokines that control IL-23-producing monocytes. Whereas Mendelian genetic defects in IL-10 receptor signalling induced IL-23 secretion after lipopolysaccharide stimulation, whole bacteria exposure induced IL-23 production in controls via acquired IL-10 signalling resistance. We found a transcriptional signature of IL-23-producing inflammatory monocytes that predicted both disease and resistance to antitumour necrosis factor (TNF) therapy and differentiated that from an IL-23-associated lymphocyte differentiation signature that was present in homeostasis and in disease.ConclusionOur work identifies IL-10 and IL-1 as critical regulators of monocyte IL-23 production. We differentiate homeostatic IL-23 production from hyperinflammation-associated IL-23 production in patients with severe ulcerating active Crohn’s disease and anti-TNF treatment non-responsiveness. Altogether, we identify subgroups of patients with IBD that might benefit from IL-23p19 and/or IL-1α/IL-1β-targeting therapies upstream of IL-23.

scholarly journals AB0042 CYTOKINE NETWORK ELUCIDATED BY THE QUANTIFICATION OF MULTIPLE CYTOKINES IN THE SERUM SEQUENTIALLY SAMPLED FROM RA PATIENTS WHO WERE TREATED WITH BIOLOGIC DMARDS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1323.2-1324
Author(s):  
K. Sato ◽  
S. Mamada ◽  
C. Hayashi ◽  
T. Nagashima ◽  
S. Minota
Keyword(s):  
Bone Erosion ◽  
Feedback System ◽  
Serum Levels ◽  
Type I Interferons ◽  
Type I ◽  
Serum Samples ◽  
Cytokine Network ◽  
Biologic Dmards ◽  
Type I Ifns ◽  
Before And After

Background:Biologic disease modifying anti-rheumatic drugs (DMARDs) have demonstrated that proinflammatory cytokines such as interleukin (IL-) 6 and tumor necrosis factor (TNF) play important roles in the pathogenesis of rheumatoid arthritis (RA). Other cytokines, such as type I interferons (IFNs), are also implicated in its pathogenesis (ref 1). However, the complete picture of the cytokine network involved in RA remains to be elucidated.Objectives:By quantifying sets of cytokines in the serum of RA patients before and after treatment with various biologic DMARDs, we sought to determine the effects of drugs on (A) type I IFNs, (B) soluble IL-6 receptors, and (C) other cytokines.Methods:52 patients with RA were treated with various biologic DMARDs (tocilizumab (TOC): 16, abatacept (ABT): 15, and TNF inhibitors (TNFi): 21). Serum samples were obtained (1) before, (2) approximately 4 weeks after (3) and approximately 12 weeks after the initiation of treatment. A suspension bead-array system was used for analysis; Bio-Plex Human Cytokine 17-plex Assay kits and Express Custom Panels (Bio-Rad), including IFN-β, IFN-α2, soluble IL-6 receptor α (sIL6Rα) and gp130 were used.Results:(1) As expected, the disease activity score 28-joiny count (DAS28) using the erythrocyte sedimentation rate (ESR) significantly decreased in all three groups (TOC, ABT and TNFi) by 12 weeks.(2) IFN-α2 was barely detected in the serum samples. IFN-β seemed to increase slightly in the ABT group, but the increase was not statistically significant.(3) The levels of sIL6Rα did not change substantially. Those of gp130 decreased slightly but significantly in the TOC group by 12 weeks.(4) The levels of IL-6 decreased significantly in the ABT group by 12 weeks. Those in the TNFi group decreased significantly at 4 weeks but not 12 weeks (Fig. 1A).(5) The levels of IL-7 decreased significantly only in the TOC group (Fig. 1B).Conclusion:(1) The biologic DMARDs tested in this study did not significantly affect the serum levels of type I IFNs in this study.(2) The decrease in gp130 in the TOC group may imply that gp130 is induced by IL-6, although whether this level of decrease has physiological significance is open to question.(3) Serum IL-6 was significantly decreased in the TNFi group at 4 weeks but not 12 weeks. TNF has been reported to induce IL-6 (ref 2), but negative feedback loop(s) may be present. Such a feedback system might make the discontinuation of TNFi difficult, even if patients are in remission.(4) IL-7 may be a target of IL-6. A higher level of IL-7 has been reported to be present in the joints of RA patients compared with osteoarthrosis and it is a cytokine implicated in the differentiation of osteoclasts (ref 3). This may partly explain the effect of TOC on preventing bone erosion in RA.References:[1]Ann Rheum Dis. 2007; 66: 1008–14[2]Rheumatology 2007; 46: 920-6[3]Rheumatology 2008; 47: 753-9Acknowledgments:We thank all the members of the Division of Rheumatology and Clinical Immunology, Department of Medicine, Jichi Medical University. We are also grateful to the patients involved in this study.Disclosure of Interests:Kojiro Sato Grant/research support from: Abbie, Pfizer, Chugai, Astellas, Mitsubishi-Tanabe, Ono, Takeda, Sachiko Mamada: None declared, Chiyomi Hayashi: None declared, Takao Nagashima: None declared, Seiji Minota: None declared

The 795CT polymorphism in osteopontin gene is not associated with multiple sclerosis in a Spanish population

2007 ◽  
Vol 13 (2) ◽  
pp. 250-252 ◽  
Author(s):  
A Mas ◽  
A Martínez ◽  
V De Las Heras ◽  
M Bartolomé ◽  
Eg De La Concha ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Low Frequency ◽  
Interleukin 10 ◽  
Interleukin 12 ◽  
Italian Population ◽  
Cytokine Network ◽  
Activated T Cells ◽  
Negative Finding ◽  
The Central Nervous System ◽  
Ms Pathogenesis

Multiple sclerosis (MS) is an inflammatory disease affecting the central nervous system. The dysregulation of the cytokine network is an important component of its pathogenesis. One of the cytokines produced by activated T-cells is osteopontin (OPN). OPN enhances the production of the pro-inflammatory cytokines, interleukin-12 and interferon-gamma, while reducing interleukin-10 levels. Therefore, OPN is considered a pro-inflammatory cytokine, and could play a key role in MS pathogenesis. The OPN gene contains several common polymorphisms, distributed in two main haplotypes, which may modulate its production or activity. A total of 326 MS patients and 484 healthy controls were typed for 795CT OPN polymorphism. In order to perform a familial study, 51 progenitor pairs were also included. No difference was found in the case-control or family study. This negative finding is inconsistent with a previous haplotype study in an Italian population, where the haplotype associated carried the low-frequency allele in position 795. In a Japanese population, a similar study yielded no association with this polymorphism. In conclusion, our data suggest that the 795 polymorphism does not play an etiological role per se and the haplotype structure may differ from one population to another. Multiple Sclerosis 2007; 13: 250–252. http://msj.sagepub.com

The effects of vitamin B on the immune/cytokine network and their involvement in depression

Maturitas ◽  
2017 ◽  
Vol 96 ◽  
pp. 58-71 ◽  
Author(s):  
Kathleen Mikkelsen ◽  
Lily Stojanovska ◽  
Monica Prakash ◽  
Vasso Apostolopoulos
Keyword(s):  
Vitamin B ◽  
Cytokine Network

scholarly journals Evidence for an Epidermal Cytokine Network

1990 ◽  
Vol 95 (6) ◽  
pp. S100-S104 ◽  
Author(s):  
Thomas A. Luger ◽  
Thomas Schwarz
Keyword(s):  
Cytokine Network
Sign in / Sign up

Export Citation Format

Share Document