Genomics in MEGene variants of IL12B, IL1B and IL4R have been identified as a risk loci in ME (1):
Cytokines in ME
Plasma cytokine levels have been measured in ME patients with short-duration illness (≤3 years) and ME patients with long-duration illness (>3 years) (2).
IL-12B (IL-12p40) was increased in short-duration and decreased in long-duration compared to normal controls.
IL-1β was decreased in long-duration compared to short-duration and normal controls (2).
IL4 was increased in short-duration and decreased in long-duration compared to normal controls (2).
Interferon-γ (IFNγ) was decreased in long-duration compared to short-duration and normal controls (2).
Cytokines and IDO1IL-12B stimulate the production of IFNγ, and IFNγ induce IDO1 activity (3).
IDO1 is inhibited by IL-4 (3).
Do the risk loci play a role in the ME-IDO-metabolic trap hypothesis?
Further reading:Genomics, proteomics and transcriptomics show the iNOS pathway is upregulated in ME
References:1) Whole Genome Sequencing and Analysis of ME/CFS https://www.youtube.com/watch?v=nIJX-Q7w_Z4
2) Hornig et al: Distinct plasma immune signatures in ME/CFS are present early in the course of illness. Sci Adv. 2015 Feb;1(1). pii: e1400121. https://www.ncbi.nlm.nih.gov/pubmed/26079000
3) Opitz et al: Tryptophan degradation in autoimmune diseases. Cell Mol Life Sci. 2007 Oct;64(19-20):2542-63. https://www.ncbi.nlm.nih.gov/pubmed/17611712
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