Decreased serum levels of sCD40L and IL-31 correlate in treated patients with Relapsing-Remitting Multiple Sclerosis

Guerrero-García, José de Jesús; Rojas-Mayorquín, Argelia E.; Valle, Yeminia; Padilla-Gutiérrez, Jorge Ramón; Castañeda-Moreno, V.A.; Mireles-Ramírez, Mario Alberto; Muñoz‐Valle, José Francisco; Ortuño-Sahagún, Daniel

doi:10.1016/j.imbio.2017.10.001

Cited by 22 publications

(16 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Guerrero-García et al demonstrated that the soluble form of CD40L was an excellent marker for inflammatory and autoimmune diseases. Furthermore, they found in serum the positive and close correlation between IL-31 and autoimmune diseases like multiple sclerosis [ 55 ].…”

Section: Il-31 and Il-33 In Diseasesmentioning

confidence: 99%

IL-33/IL-31 Axis: A Potential Inflammatory Pathway

Salvo

Ventura-Spagnolo

Casciaro

et al. 2018

Mediators of Inflammation

View full text Add to dashboard Cite

Cytokines play an important role in the regulation of the immune system (adaptive and innate). Given their importance in proinflammatory processes, cytokines have been used for understanding the pathogenesis and as biomarkers in many diseases. IL-31 and IL-33 are still considered novel cytokines. IL-31 controls signalling and regulates a huge amount of biological functions: it induces proinflammatory cytokines, regulates cell proliferation, and is involved also in tissue remodelling. On the other hand, IL-33 has been identified as an "alarmin" released from the epithelial cells and from different human tissues and organs after a damage following, that is, an inflammatory process. The aim of this literature review is to strengthen the hypothesis about an IL-31/IL-33 axis by evaluating the most recent studies linking these two cytokines. Literature data showed that, in many cases, IL-31 and IL-33 are linked to each other and that their expression is correlated with disease severity. The presence of one interleukin might stimulate the induction of the other, amplifying inflammation and the consequent detrimental processes. In a near future, influencing their balance could be helpful in modulating the first responses of the immune system in order to prevent the development of many inflammation-related diseases.

show abstract

Section: Il-31 and Il-33 In Diseasesmentioning

confidence: 99%

IL-33/IL-31 Axis: A Potential Inflammatory Pathway

Salvo

Ventura-Spagnolo

Casciaro

et al. 2018

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…Although serum sCD40L concentrations, but not CSF sCD40L concentrations, positively correlated (Kendall tau- b = 0.29, p = 0.044) with the CSF/serum albumin ratio (“Qalb”), an indicator of blood-brain barrier permeability ( 33 ), it is currently unknown whether sCD40L directly contributes to BBB breakdown. Interestingly, serum concentrations of sCD40L decreased upon treatment with Glatiramer acetate (copaxone) ( 34 ), IFN-β ( 35 ), or natalizumab ( 36 ), suggesting that sCD40L can be used as a biomarker to monitor the effectiveness of these therapies.…”

Section: Expression Of Cd40l During Msmentioning

confidence: 99%

The CD40–CD40L Dyad in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis

et al. 2017

View full text Add to dashboard Cite

The CD40–CD40L dyad is an immune checkpoint regulator that promotes both innate and adaptive immune responses and has therefore an essential role in the development of inflammatory diseases, including multiple sclerosis (MS). In MS, CD40 and CD40L are expressed on immune cells present in blood and lymphoid organs, affected resident central nervous system (CNS) cells, and inflammatory cells that have infiltrated the CNS. CD40–CD40L interactions fuel the inflammatory response underlying MS, and both genetic deficiency and antibody-mediated inhibition of the CD40–CD40L dyad reduce disease severity in experimental autoimmune encephalomyelitis (EAE). Both proteins are therefore attractive therapeutic candidates to modulate aberrant inflammatory responses in MS. Here, we discuss the genetic, experimental and clinical studies on the role of CD40 and CD40L interactions in EAE and MS and we explore novel approaches to therapeutically target this dyad to combat neuroinflammatory diseases.

show abstract

“…Interferon-β is a first-line immunomodulatory treatment in relapsing–remitting (RR)-MS and shows beneficial effects on disease progression reducing the frequency and severity of clinical exacerbations ( 18 ). Its mechanisms of action include modulatory effects on costimulatory molecules ( 19 ) and shift from Th1 to Th2 cytokine production ( 20 – 26 ), and other studies have suggested modulation of Th17 development ( 27 – 29 ).…”

Section: Introductionmentioning

confidence: 99%

Profiling of Canonical and Non-Traditional Cytokine Levels in Interferon-β-Treated Relapsing–Remitting-Multiple Sclerosis Patients

et al. 2018

View full text Add to dashboard Cite

BackgroundMultiple sclerosis (MS) is a chronic, progressive autoimmune disease of the central nervous system in which inflammation plays a key role in the induction, development, and progression. Most of the MS patients present with relapsing–remitting (RR) form, characterized by flare-ups followed by periods of recovery. Many inflammatory and anti-inflammatory cytokines have been proposed as backers in MS pathogenesis, and the balance between these differing cytokines can regulate MS severity. Interferon (IFN)-β, a current disease-modifying therapy for MS, has demonstrated beneficial effects in reducing disease severity in MS patients. However, its immunoregulatory and anti-inflammatory actions in MS are not wholly understood. The aim of the study was to define, in clinically stable patients with RR-MS, the serum concentration of several cytokines, canonical or not, and their modulation by IFN-β therapy.MethodsRelapsing–remitting-MS patients were enrolled and diagnosed according to revised Mc Donald Diagnostic Criteria. A set of cytokines [including non-canonical neurotransmitter acetylcholine (ACh) and adipokines] and B-cell differentiation molecules, as potential biomarkers, were evaluated in 30 non-treated RR-MS patients compared to 30 IFN-β-treated MS patients and 30 age, gender, and body mass index-matched healthy controls (HC).ResultsNaïve MS patients showed significantly higher levels of interleukin (IL)-1β, IL-12/IL-23p40, IL-18, high-mobility group box protein-1, and IL-18 binding protein (IL-18BP) than MS-treated patients (p < 0.001 for all) and HC (p < 0.01). IFN-β therapy has significantly downmodulated IL-1β, IL-12/IL-23p40, IL-18 to normal levels (p < 0.001), whereas it has decreased IL-18BP (p < 0.001). ACh was significantly higher in the IFN-β-treated than HC and non-treated MS patients (p < 0.001). No significant differences were observed either in adipokines concentration or in B-cell-associated molecules among the three study groups.ConclusionAlthough more experimental evidence are required, we speculate that the efficacy of treatment of MS with IFN-β is mediated, at least in part, by its ability to work on several levels to slow down the disease progression. Proposed actions include the modulation of IL-1–inflammasome axis and modulation of ACh, B-cell activating factor/a proliferation-inducing ligand system, and several adipokines.

show abstract

Decreased serum levels of sCD40L and IL-31 correlate in treated patients with Relapsing-Remitting Multiple Sclerosis

Cited by 22 publications

References 65 publications

IL-33/IL-31 Axis: A Potential Inflammatory Pathway

IL-33/IL-31 Axis: A Potential Inflammatory Pathway

The CD40–CD40L Dyad in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis

Profiling of Canonical and Non-Traditional Cytokine Levels in Interferon-β-Treated Relapsing–Remitting-Multiple Sclerosis Patients

Contact Info

Product

Resources

About