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IL-22 Binding Protein Promotes the Disease Process in Multiple Sclerosis.

Hannes Lindahl1, André O Guerreiro-Cacais2, Sahl Khalid Bedri2

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Multiple sclerosis (MS) risk variant rs17066096 is linked to increased IL-22 binding protein (IL-22BP). Higher IL-22BP levels correlate with MS disease severity, suggesting IL-22BP

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Area of Science:

  • Neuroimmunology
  • Genetics
  • Immunology

Background:

  • Genome-wide association studies identify genetic variants predisposing to multiple sclerosis (MS).
  • The pathogenic mechanisms underlying MS genetic risk factors remain poorly understood.
  • Interleukin-22 (IL-22) is a cytokine involved in immune regulation, and its antagonist, IL-22 binding protein (IL-22BP), is a potential therapeutic target.

Purpose of the Study:

  • To investigate the role of the MS genetic risk variant rs17066096 and its associated gene, IL-22BP, in MS pathogenesis.
  • To explore the functional consequences of IL-22BP expression in MS.
  • To elucidate the potential therapeutic implications of targeting the IL-22 pathway in MS.

Main Methods:

  • Genotyping of the rs17066096 risk variant.
  • In vitro expression analysis of IL-22BP in monocytes from risk genotype carriers.
  • Measurement of IL-22BP levels in cerebrospinal fluid and correlation with MS lesion load.
  • Validation of IL-22BP pathogenicity in rat and mouse models of MS.
  • Investigation of the mechanism involving T cell-derived IFN-γ expression.

Main Results:

  • Monocytes from carriers of the rs17066096 risk genotype exhibit increased IL-22BP expression in vitro.
  • Cerebrospinal fluid IL-22BP levels positively correlate with MS lesion load on MRI.
  • IL-22BP demonstrates pathogenicity in rat and mouse models of MS.
  • A proposed pathogenic mechanism involves impaired IL-22-mediated inhibition of T cell-derived IFN-γ.

Conclusions:

  • The genetic risk variant rs17066096 is associated with increased IL-22BP, a key player in MS pathogenesis.
  • IL-22BP contributes to MS pathology across species, potentially through modulation of T cell responses.
  • Targeting IL-22BP or enhancing IL-22 activity presents a potential therapeutic strategy for MS.