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{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4419340","sourcedb":"PMC","sourceid":"4419340","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4419340","text":"Normal cellular responses to fungal compounds\nFinally, we investigated IL-6, IFN-γ, and IL-17A production by P2’s whole blood upon 48 h of stimulation with fungal compounds (Curdlan, heat-killed C. albicans, Saccharomyces cerevisiae, and Exophiala dermatitidis), as well as heat-killed Staphylococcus aureus, vesicular stomatitis virus (VSV), bacillus Calmette–Guérin (BCG), and PMA/ionomycin. The levels of all three cytokines produced were comparable with those obtained after whole blood stimulation of a local or a travel control (Fig. 9, A–C). Similarly, monocyte-derived DCs (MDDCs) from P2, P3, and their relatives, activated with various fungal compounds (including zymosan, heat-killed S. cerevisiae, C. albicans, E. dermatitidis, and Curdlan), as well as VSV, BCG, or LPS, produced levels of TNF comparable with the healthy controls tested in the same conditions (Fig. 10, A and B). Altogether, these results suggest that IL-17RC deficiency does not impair the whole blood or MDDC response to fungal compounds, at least for the cytokines measured, including IL-17A. Altogether, these data suggest that the patients’ defective IL-17RC–dependent responsive pathway is primarily responsible for CMC, as it does not affect the production of IL-17A and other cytokines by leukocytes and MDDCs in response to stimulation by C. albicans.\nFigure 9. Normal IL-6, IFN-γ, and IL-17A production by P2’s whole blood upon 48 h of stimulation with fungal compounds. (A–C) Whole blood from a local control (white bars), a travel control (gray bars), and P2 (black bars) were stimulated with fungal compounds (Curdlan, heat-killed C. albicans, S. cerevisiae, E. dermatitidis: a black yeast), as well as heat-killed S. aureus, VSV, BCG, or PMA/ionomycin for 48 h. IL-6 (A), IFN-γ (B), and IL-17A (C) were measured by ELISA. The experiments were repeated two times.\nFigure 10. Normal TNF production by P2’s and P3′s MDDCs upon 48 h of stimulation with fungal compounds. (A and B) MDDCs from four healthy control individuals (white bars), four heterozygous patients’ relatives (gray bars), and P2 or P3 (black bars) were stimulated with fungal compounds (zymosan, heat-killed S. cerevisiae [HKSC], C. albicans [HKCA and SC5314], E. dermatitidis, and Curdlan), as well as with VSV, BCG, or LPS for 48 h. TNF was measured by ELISA. Error bars represent SEM. The experiments were repeated two times.\n\nD","divisions":[{"label":"Title","span":{"begin":0,"end":45}},{"label":"Figure caption","span":{"begin":1341,"end":1859}},{"label":"Figure caption","span":{"begin":1858,"end":2390}}],"tracks":[]}