Highlights
- •Serum ILs-22, 32α and 34 concentrations were assessed in multiple sclerosis.
- •Serum IL-22 concentration positively correlated with EDSS value.
- •Serum IL-22 concentration negatively correlated with the treatment duration.
- •Serum IL-22 concentration may be a potential marker for multiple sclerosis severity.
- •Serum IL-22 concentration may be a good predictor of treatment efficacy.
Abstract
Interleukins (ILs)-22, 32α and 34 were monitored in the sera of relapsing-remitting
multiple sclerosis (RRMS) patients at different time intervals with or without interferon
β-1b, interferon β-1a and fingolimod treatments. The results showed that sera of untreated
RRMS patients were statistically higher in concentration of IL-22 (P < .001), but not IL-32α and IL-34, than those of healthy individuals. Interestingly,
interferon β-1b, interferon β-1a and fingolimod treatments led to a significant decrease
of serum concentrations of ILs-22 and 32α, but not 34, at 6 and 12 months of treatment,
compared to their initial concentrations before initiating therapy. The correlation
analysis revealed that the changes of serum IL-22 (r = 0.814) and, to a lesser extent, IL-32α (r = 0.381) concentrations were positively correlated with those of expanded disability
status score. In conclusion, serum IL-22 concentration may be a potential marker for
MS disease severity and efficacy of treatment.
Graphical abstract

Graphical Abstract
Keywords
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References
- Increase in Th17 and T-reg lymphocytes and decrease of IL22 correlate with the recovery phase of acute EAE in rat.PLoS One. 2011; 6 (:e27473-e)
- Identification of a novel gene expressed in activated natural killer cells and T cells.Journal of immunology (Baltimore, Md : 1950). 1992; 148: 597-603
- Stroma-derived interleukin-34 controls the development and maintenance of langerhans cells and the maintenance of microglia.Immunity. 2012; 37: 1050-1060
- Clinical significance of interleukin-32 expression in patients with rheumatoid arthritis.Asian Pac. J. Allergy Immunol. 2013; 31: 73-78
- Amelioration of experimental autoimmune encephalomyelitis by plumbagin through down-regulation of JAK-STAT and NF-kappaB signaling pathways.PLoS One. 2011; 6e27006
- Interleukin-34 restores blood-brain barrier integrity by upregulating tight junction proteins in endothelial cells.PLoS One. 2014; 9 (e115981-e)
- IL-32gamma induces the maturation of dendritic cells with Th1- and Th17-polarizing ability through enhanced IL-12 and IL-6 production.Journal of immunology (Baltimore, Md : 1950). 2011; 186: 6848-6859
- Human TH17 lymphocytes promote blood-brain barrier disruption and central nervous system inflammation.Nat. Med. 2007; 13: 1173-1175
- Interleukin-22 promotes osteoclastogenesis in rheumatoid arthritis through induction of RANKL in human synovial fibroblasts.Arthritis Rheum. 2012; 64: 1015-1023
- Neuroinflammation, neurodegeneration and regeneration in multiple sclerosis: intercorrelated manifestations of the immune response.Neural Regen. Res. 2016; 11: 1727-1730
- Interleukin-22 (IL-22) activates the JAK/STAT, ERK, JNK, and p38 MAP kinase pathways in a rat hepatoma cell line. Pathways that are shared with and distinct from IL-10.The Journal of biological chemistry. 2002; 277: 33676-33682
- Colony-stimulating factor 1 receptor (CSF1R) signaling in injured neurons facilitates protection and survival.J. Exp. Med. 2013; 210: 157-172
- TGF-beta induced by interleukin-34-stimulated microglia regulates microglial proliferation and attenuates oligomeric amyloid beta neurotoxicity.Neurosci. Lett. 2012; 529: 86-91
- Th17 cells: biology, pathogenesis of autoimmune and inflammatory diseases, and therapeutic strategies.Am. J. Pathol. 2012; 181: 8-18
- Interleukin-34 selectively enhances the neuroprotective effects of microglia to attenuate oligomeric amyloid-beta neurotoxicity.Am. J. Pathol. 2011; 179: 2016-2027
- Association between interleukin-32 polymorphism and multiple sclerosis.J. Neurol. Sci. 2017; 379: 144-150
- Elevated serum level of interleukin-32alpha in the patients with myasthenia gravis.J. Neurol. 2011; 258: 1865-1870
- Endogenous IL-32 controls cytokine and HIV-1 production.Journal of immunology (Baltimore, Md : 1950). 2008; 181: 557-565
- IL-32-dependent effects of IL-1beta on endothelial cell functions.Proc. Natl. Acad. Sci. U. S. A. 2009; 106: 3883-3888
- The link of inflammation and neurodegeneration in progressive multiple sclerosis.Multiple Sclerosis and Demyelinating Disorders. 2016; 1: 9
- Interleukin-22 is increased in multiple sclerosis patients and targets astrocytes.J. Neuroinflammation. 2015; 12: 119
- Th22 cells are expanded in multiple sclerosis and are resistant to IFN-beta.J. Leukoc. Biol. 2014; 96: 1155-1164
- Identification of a human helper T cell population that has abundant production of interleukin 22 and is distinct from T(H)-17, T(H)1 and T(H)2 cells.Nat. Immunol. 2009; 10: 864-871
- Interkeukin-34, a cytokine crucial for the differentiation and maintenance of tissue resident macrophages and Langerhans cells.Eur. J. Immunol. 2014; 44: 1575-1581
- Increased plasma interleukin-32 expression in patients with neuromyelitis optica.J. Clin. Immunol. 2013; 33: 666-670
- Association of Plasma IL-32 levels and gene polymorphisms with systemic lupus erythematosus in Chinese Han population.Dis. Markers. 2016; 20162460206
- Interleukin-17- and interleukin-22-secreting myelin-specific CD4(+) T cells resistant to corticoids are related with active brain lesions in multiple sclerosis patients.Immunology. 2016; 147: 212-220
- IL-22 secreting CD4+ T cells in the patients with neuromyelitis optica and multiple sclerosis.J. Neuroimmunol. 2013; 261: 87-91
- Interleukin-22: a likely target for treatment of autoimmune diseases.Autoimmun. Rev. 2014; 13: 615-620
- Myelin oligodendrocyte glycoprotein (MOG35-55)-induced experimental autoimmune encephalomyelitis is ameliorated in interleukin-32 alpha transgenic mice.Oncotarget. 2015; 6: 40452-40463
- IL-22 promotes Fas expression in oligodendrocytes and inhibits FOXP3 expression in T cells by activating the NF-kappaB pathway in multiple sclerosis.Mol. Immunol. 2017; 82: 84-93
Article info
Publication history
Published online: September 06, 2019
Accepted:
September 5,
2019
Received in revised form:
August 29,
2019
Received:
April 9,
2019
Identification
Copyright
© 2019 Elsevier B.V. All rights reserved.