Disease relevance of C19orf10

• IL-25-induced eosinophilia required IL-5 and IL-13, but not IL-4 or T cells [1].
• Mice given intranasal IL-25 also developed epithelial cell hyperplasia, increased mucus secretion, and airway hyperreactivity [1].
• We have generated IL-25-deficient (il25(-/-)) mice and found that they are highly susceptible to experimental autoimmune encephalomyelitis (EAE) [2].
• New evidence shows that the IL-17-related cytokine IL-25 is essential for Th2 responses in two infectious disease models [3].
• The SF-20 and SF-36 were also used to compare headache disorders with other chronic illnesses [4].

Psychiatry related information on C19orf10

• Functional status was assessed by questionnaires characterizing walking ability (Walking Impairment Questionnaire, WIQ), habitual physical activity level (Physical Activity Recall, PAR), and physical, social, and role functioning, well-being, and overall health (Medical Outcomes Study SF-20, MOS) [5].
• A short, psychiatric, case-finding measure for HIV seropositive outpatients: performance characteristics of the 5-item mental health subscale of the SF-20 in a male, seropositive sample [6].
• Gender differences in patients with bipolar disorder influence outcome in the medical outcomes survey (SF-20) subscale scores [7].

High impact information on C19orf10

• We now show that IL-25 also regulates the development of autoimmune inflammation mediated by IL-17-producing T cells [2].
• Thus, IL-25 and IL-17, being members of the same cytokine family, play opposing roles in the pathogenesis of organ-specific autoimmunity [2].
• Interleukin 25 regulates type 2 cytokine-dependent immunity and limits chronic inflammation in the gastrointestinal tract [8].
• We demonstrate that these IL-25-regulated cells appear rapidly in the draining lymph nodes, implicating them as a source of type 2 cytokines during initiation of worm expulsion [9].
• In contrast, administration of recombinant IL-25 in vivo induces the appearance of NBNT, c-kit(+), FcepsilonR1(-) cells and leads to rapid worm expulsion that is T and B cell independent, but type 2 cytokine dependent [9].

Biological context of C19orf10

• IL-25 gene expression was detected following Aspergillus and Nippostrongylus infection in the lung and gut, respectively [1].
• IL-25-induced AHR is dependent on the production of Th type-2 cytokines, and removal of IL-13 and its signal transduction pathway prevents IL-25-induced airways inflammation and AHR [10].
• IL-25 potently induces inflammatory cascades that may exacerbate allergic airways inflammation by promoting Th type-2 cytokine responses in conjunction with the up-regulation of factors (eotaxin and arg-I) that can amplify inflammation associated with allergic disorders [10].

Anatomical context of C19orf10

• RESULTS: Viability of eosinophils was significantly enhanced by IL-25 from 41% to 76% dose-dependently [11].
• Recently, it has been demonstrated that a novel IL-17 family cytokine IL-25 (IL-17E) is a product of activated Th2 cells and mast cells [12].

Associations of C19orf10 with chemical compounds

• IL-27, which could mimic the effect of IL-12, was however less potent in inducing IFN-gamma production in the presence of CsA and TCR stimulation [13].

Other interactions of C19orf10

• The association of the components of the BILAG index with health status as measured with the MOS Short Form 20 (SF-20), with patients' and doctors' global assessments of patient wellbeing and with laboratory tests was analysed with Spearman rank correlations [14].

Analytical, diagnostic and therapeutic context of C19orf10

• Health-related quality of life was assessed with the Medical Outcomes Study SF-20 General Health Survey. RESULTS: Women were more likely than men to have at least one mental disorder (43% versus 33%, P < 0.05) [15].
• METHODS: One hundred and five SLE patients completed the Medical Outcome Survey (MOS) SF-20 during their regular clinic visit [16].

References