Inhibition of IFN-γ as a Method of Treatment of Various Autoimmune Diseases, Including Skin Diseases

Skurkovich, Boris; Skurkovich, S. V.

doi:10.1007/3-540-37673-9_1

Cited by 28 publications

(25 citation statements)

References 75 publications

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“…[5,18]. IL-1b and IFN-c are recently considered being potential new targets in arthritis therapy [19][20][21]. Our study detected an increased expression of PGK1 in RA synovial tissues.…”

Section: Discussionsupporting

confidence: 63%

PGK1, a glucose metabolism enzyme, may play an important role in rheumatoid arthritis

Zhao

Yan

et al. 2016

Inflamm. Res.

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“…[5,18]. IL-1b and IFN-c are recently considered being potential new targets in arthritis therapy [19][20][21]. Our study detected an increased expression of PGK1 in RA synovial tissues.…”

Section: Discussionsupporting

confidence: 63%

PGK1, a glucose metabolism enzyme, may play an important role in rheumatoid arthritis

Zhao

Yan

et al. 2016

Inflamm. Res.

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“…A biological tailored more specifically to the AA pathogenic mechanism might be necessary to gain the greatest therapeutic benefit. Research in animal models suggests that, of the biologicals under development, anti-IFN-γ (fontolizumab) might have the most potential as an effective treatment ( Refs 156,157).…”

Section: Lymphocyte Activationmentioning

confidence: 99%

Alopecia areata: pathogenesis and potential for therapy

Shapiro

et al. 2006

Expert Rev. Mol. Med.

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Although the complete picture for alopecia areata (AA) pathogenesis has yet to be determined, recent research has made much progress in our understanding of the disease mechanism. Numerous circumstantial evidence supports the notion that AA is fundamentally a disease mediated by inflammatory cells and may be autoimmune in nature. Recent research has shown the hair-loss phenotype is precipitated predominantly by CD8+ lymphocytes, but the disease mechanism is driven by CD4+ lymphocytes. Although genetic susceptibility is a key contributor to disease development, disease onset and phenotypic presentation are probably modified by complex environmental interplay. On the basis of our current understanding of AA disease pathogenesis, several experimental and theoretical therapeutic approaches might be possible. However, the pathogenetic disease mechanism is particularly robust and the development of a cure for AA will be a significant challenge.

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“…inhibition of cytokine production by IFNG inhibiting protein (Koga et al 2007), antibodies to TNF-alpha and IFNG (Skurkovich and Skurkovich 2006) and by antidepressants, e.g., selective 5-HT inhibitor, fluoxetine (Kenis and Maes 2002) and dopamine enhancer, wellbutrin (Brustolim et al 2006)…”

Section: Inhibition Of Try–kyn/guanine–pteridines Metabolism As a Newmentioning

confidence: 99%

Interferon-gamma-inducible kynurenines/pteridines inflammation cascade: implications for aging and aging-associated psychiatric and medical disorders

2010

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This review of literature and our data suggests that up-regulated production of interferon-gamma (IFNG) in periphery and brain triggers a merger of tryptophan (TRY)–kynurenine (KYN) and guanine–tetrahydrobiopterin (BH4) metabolic pathways into inflammation cascade involved in aging and aging-associated medical and psychiatric disorders (AAMPD) (metabolic syndrome, depression, vascular cognitive impairment). IFNG-inducible KYN/pteridines inflammation cascade is characterized by up-regulation of nitric oxide synthase (NOS) activity (induced by KYN) and decreased formation of NOS cofactor, BH4, that results in uncoupling of NOS that shifting arginine from NO to superoxide anion production. Superoxide anion and free radicals among KYN derivatives trigger phospholipase A2-arachidonic acid cascade associated with AAMPD. IFNG-induced up-regulation of indoleamine 2,3-dioxygenase (IDO), rate-limiting enzyme of TRY–KYN pathway, decreases TRY conversion into serotonin (substrate of antidepressant effect) and increases production of KYN associated with diabetes [xanthurenic acid (XA)], anxiety (KYN), psychoses and cognitive impairment (kynurenic acid). IFNG-inducible KYN/pteridines inflammation cascade is impacted by IFNG (+874) T/A genotypes, encoding cytokine production. In addition to literature data on KYN/TRY ratio (IDO activity index), we observe neopterin levels (index of activity of rate-limiting enzyme of guanine–BH4 pathway) to be higher in carriers of high (T) than of low (A) producers alleles; and to correlate with AAMPD markers (e.g., insulin resistance, body mass index, mortality risk), and with IFN-alpha-induced depression in hepatitis C patients. IFNG-inducible cascade is influenced by environmental factors (e.g., vitamin B6 deficiency increases XA formation) and by pharmacological agents; and might offer new approaches for anti-aging and anti-AAMPD interventions.

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Inhibition of IFN-γ as a Method of Treatment of Various Autoimmune Diseases, Including Skin Diseases

Cited by 28 publications

References 75 publications

PGK1, a glucose metabolism enzyme, may play an important role in rheumatoid arthritis

PGK1, a glucose metabolism enzyme, may play an important role in rheumatoid arthritis

Alopecia areata: pathogenesis and potential for therapy

Interferon-gamma-inducible kynurenines/pteridines inflammation cascade: implications for aging and aging-associated psychiatric and medical disorders

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