Impact of Immunomodulatory Treatment on Leukocyte Cytokine Production in Multiple Sclerosis Patients and Healthy Donors

2009 ◽  
Vol 16 (6) ◽  
pp. 385-391 ◽  
Author(s):  
Dirk Reske ◽  
Anne V. Thomas ◽  
Hela-Felicitas Petereit ◽  
Gereon R. Fink ◽  
Michael Schroeter
Keyword(s):  
Multiple Sclerosis ◽  
Cytokine Production ◽  
Immunomodulatory Treatment ◽  
Healthy Donors ◽  
Multiple Sclerosis Patients

CRYAB modulates the activation of CD4+ T cells from relapsing–remitting multiple sclerosis patients

2013 ◽  
Vol 19 (14) ◽  
pp. 1867-1877 ◽  
Author(s):  
Que Lan Quach ◽  
Luanne M Metz ◽  
Jenna C Thomas ◽  
Jonathan B Rothbard ◽  
Lawrence Steinman ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cells ◽  
Cytokine Production ◽  
Clinical Signs ◽  
Healthy Controls ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Multiple Sclerosis Patients ◽  
Relapsing Remitting Multiple Sclerosis

Background: Suppression of activation of pathogenic CD4+ T cells is a potential therapeutic intervention in multiple sclerosis (MS). We previously showed that a small heat shock protein, CRYAB, reduced T cell proliferation, pro-inflammatory cytokine production and clinical signs of experimental allergic encephalomyelitis, a model of MS. Objective: We assessed whether the ability of CRYAB to reduce the activation of T cells translated to the human disease. Methods: CD4+ T cells from healthy controls and volunteers with MS were activated in vitro in the presence or absence of a CRYAB peptide (residues 73–92). Parameters of activation (proliferation rate, cytokine secretion) and tolerance (anergy, activation-induced cell death, microRNAs) were evaluated. Results: The secretion of pro-inflammatory cytokines by CD4+ T cells was decreased in the presence of CRYAB in a subset of relapsing–remitting multiple sclerosis (RRMS) participants with mild disease severity while no changes were observed in healthy controls. Further, there was a correlation for higher levels of miR181a microRNA, a marker upregulated in tolerant CD8+ T cells, in CD4+ T cells of MS patients that displayed suppressed cytokine production (responders). Conclusion: CRYAB may be capable of suppressing the activation of CD4+ T cells from a subset of RRMS patients who appear to have less disability but similar age and disease duration.

Stressor-Induced Alteration of Cytokine Production in Multiple Sclerosis Patients and Controls

1998 ◽  
Vol 60 (4) ◽  
pp. 484-491 ◽  
Author(s):  
Kurt D. Ackerman ◽  
Michael Martino ◽  
Rock Heyman ◽  
Niall M. Moyna ◽  
Bruce S. Rabin
Keyword(s):  
Multiple Sclerosis ◽  
Cytokine Production ◽  
Multiple Sclerosis Patients

Single-cell analysis of cytokine production shows different immune profiles in multiple sclerosis patients with active or quiescent disease

2001 ◽  
Vol 121 (1-2) ◽  
pp. 88-101 ◽  
Author(s):  
Mario Clerici ◽  
Marina Saresella ◽  
Daria Trabattoni ◽  
Livianna Speciale ◽  
Sabrina Fossati ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Single Cell ◽  
Cytokine Production ◽  
Single Cell Analysis ◽  
Cell Analysis ◽  
Multiple Sclerosis Patients ◽  
Quiescent Disease

CCL2 induction by 1,25(OH)2D3 in dendritic cells from healthy donors and multiple sclerosis patients

2014 ◽  
Vol 144 ◽  
pp. 102-105 ◽  
Author(s):  
Isabella Sanseverino ◽  
Arturo O. Rinaldi ◽  
Cristina Purificato ◽  
Antonio Cortese ◽  
Enrico Millefiorini ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Dendritic Cells ◽  
Healthy Donors ◽  
Multiple Sclerosis Patients

scholarly journals Distinct Expression of Inflammatory Features in T Helper 17 Cells from Multiple Sclerosis Patients

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 533 ◽  
Author(s):  
Alessia Capone ◽  
Manuela Bianco ◽  
Gabriella Ruocco ◽  
Marco De Bardi ◽  
Luca Battistini ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cells ◽  
Cd4 T Cells ◽  
Th17 Cells ◽  
Chronic Inflammatory Disease ◽  
T Helper ◽  
T Helper 17 ◽  
Inflammatory Status ◽  
Healthy Donors ◽  
Multiple Sclerosis Patients

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). T helper (Th) 17 lymphocytes play a role in the pathogenesis of MS. Indeed, Th17 cells are abundant in the cerebrospinal fluid and peripheral blood of MS patients and promote pathogenesis in the mouse model of MS. To gain insight into the function of Th17 cells in MS, we tested whether Th17 cells polarized from naïve CD4 T cells of healthy donors and MS patients display different features. To this end, we analysed several parameters that typify the Th17 profile during the differentiation process of naïve CD4 T cells obtained from relapsing-remitting (RR)-MS patients (n = 31) and healthy donors (HD) (n = 28). Analysis of an array of cytokines produced by Th17 cells revealed that expression of interleukin (IL)-21, tumour necrosis factor (TNF)-β, IL-2 and IL-1R1 is significantly increased in Th17 cells derived from MS patients compared to healthy donor-derived cells. Interestingly, IL-1R1 expression is also increased in Th17 cells circulating in the blood of MS patients compared to healthy donors. Since IL-2, IL-21, TNF-β, and IL-1R1 play a crucial role in the activation of immune cells, our data indicate that high expression of these molecules in Th17 cells from MS patients could be related to their high inflammatory status.

The balance of pro-inflammatory and trophic factors in multiple sclerosis patients: effects of acute relapse and immunomodulatory treatment

2011 ◽  
Vol 17 (7) ◽  
pp. 851-866 ◽  
Author(s):  
Sabine Lindquist ◽  
Sarah Hassinger ◽  
Jonathan A Lindquist ◽  
Michael Sailer
Keyword(s):  
Multiple Sclerosis ◽  
Neurotrophic Factor ◽  
Biological Effects ◽  
Trophic Factors ◽  
Interactive Effects ◽  
High Dose ◽  
Immunomodulatory Treatment ◽  
Class I Mhc ◽  
Acute Relapse ◽  
Multiple Sclerosis Patients

Background: In multiple sclerosis inflammation is primarily injurious to the central nervous system, but its therapeutic suppression might inhibit repair-promoting factors. Objectives: We aimed at better describing the complexity of biological effects during an acute relapse and analysed the effects of intervention with high-dose i.v. glucocorticoids and immunomodulatory treatment with interferon-beta (IFNβ). Methods: We studied the intracellular expression levels of the pro-inflammatory mediators tumour necrosis factor alpha (TNFα) and inducible nitric oxide synthase (iNOS) together with the neurotrophins ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) in freshly isolated peripheral blood mononuclear cells of multiple sclerosis patients during an acute relapse, after intervention with i.v. methylprednisolone and at baseline, using a highly quantitative flow-cytometric approach. Results: We demonstrated the expression of CNTF in human leucocytes. We showed that CNTF levels differed in acutely relapsing multiple sclerosis patients compared with controls and increased after corticosteroid treatment. CNTF can counteract the toxicity of TNFα towards oligodendrocytes and we found TNFα increased during acute relapses. Following corticosteroids, neither TNFα nor iNOS expression was reduced. Levels of BDNF were not affected by glucocorticoids, but increased during IFNβ therapy. However, IFNβ also increased the expression of iNOS and major histocompatibility complex class I (MHC-I), underlining its immunomodulatory potential. Conclusions: Multiple sclerosis patients might benefit from reparative, and not solely from anti-inflammatory, effects of glucocorticoids. Interactive effects of glucocorticoid- and IFNβ-treatment need to be considered to improve neuroprotection and remyelination resulting from immunomodulatory treatment.

Low sensitivity to glucocorticoid inhibition of in vitro Th17-related cytokine production in multiple sclerosis patients is related to elevated plasma lipopolysaccharide levels

2013 ◽  
Vol 148 (2) ◽  
pp. 209-218 ◽  
Author(s):  
Bruna Teixeira ◽  
Vera Carolina B. Bittencourt ◽  
Thais B. Ferreira ◽  
Taissa M. Kasahara ◽  
Priscila O. Barros ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cytokine Production ◽  
Elevated Plasma ◽  
Low Sensitivity ◽  
Multiple Sclerosis Patients

Interferon-Beta Treatment Differentially Alters TLR2 and TLR4-Dependent Cytokine Production in Multiple Sclerosis Patients

2019 ◽  
Vol 26 (2) ◽  
pp. 77-83
Author(s):  
Iara Barreto Neves Oliveira ◽  
Rodrigo Saar Gomes ◽  
Larissa Fonseca Gomides ◽  
Jéssica Cristina dos Santos ◽  
Marcos Alexandre Diniz Carneiro ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Interferon Beta ◽  
Cytokine Production ◽  
Multiple Sclerosis Patients

scholarly journals FAS-ligand regulates differential activation-induced cell death of human T-helper 1 and 17 cells in healthy donors and multiple sclerosis patients

2015 ◽  
Vol 6 (5) ◽  
pp. e1741-e1741 ◽  
Author(s):  
M T Cencioni ◽  
S Santini ◽  
G Ruocco ◽  
G Borsellino ◽  
M De Bardi ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cell Death ◽  
Autoimmune Diseases ◽  
Fas Ligand ◽  
Th1 Cells ◽  
T Helper ◽  
Th Cells ◽  
Activation Induced Cell Death ◽  
Healthy Donors ◽  
Multiple Sclerosis Patients

Abstract Functionally distinct T-helper (Th) subsets orchestrate immune responses. Maintenance of homeostasis through the tight control of inflammatory Th cells is crucial to avoid autoimmune inflammation. Activation-Induced Cell Death (AICD) regulates homeostasis of T cells, and it has never been investigated in human Th cells. We generated stable clones of inflammatory Th subsets involved in autoimmune diseases, such as Th1, Th17 and Th1/17 cells, from healthy donors (HD) and multiple sclerosis (MS) patients and we measured AICD. We find that human Th1 cells are sensitive, whereas Th17 and Th1/17 are resistant, to AICD. In particular, Th1 cells express high level of FAS-ligand (FASL), which interacts with FAS and leads to caspases’ cleavage and ultimately to cell death. In contrast, low FASL expression in Th17 and Th1/17 cells blunts caspase 8 activation and thus reduces cell death. Interestingly, Th cells obtained from healthy individuals and MS patients behave similarly, suggesting that this mechanism could explain the persistence of inflammatory IL-17-producing cells in autoimmune diseases, such as MS, where their generation is particularly substantial.

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