| 1. |
- Kreins, AY, et al.
(författare)
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Human TYK2 deficiency: Mycobacterial and viral infections without hyper-IgE syndrome
- 2015
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Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 212:10, s. 1641-1662
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Tidskriftsartikel (refereegranskat)abstract
- Autosomal recessive, complete TYK2 deficiency was previously described in a patient (P1) with intracellular bacterial and viral infections and features of hyper-IgE syndrome (HIES), including atopic dermatitis, high serum IgE levels, and staphylococcal abscesses. We identified seven other TYK2-deficient patients from five families and four different ethnic groups. These patients were homozygous for one of five null mutations, different from that seen in P1. They displayed mycobacterial and/or viral infections, but no HIES. All eight TYK2-deficient patients displayed impaired but not abolished cellular responses to (a) IL-12 and IFN-α/β, accounting for mycobacterial and viral infections, respectively; (b) IL-23, with normal proportions of circulating IL-17+ T cells, accounting for their apparent lack of mucocutaneous candidiasis; and (c) IL-10, with no overt clinical consequences, including a lack of inflammatory bowel disease. Cellular responses to IL-21, IL-27, IFN-γ, IL-28/29 (IFN-λ), and leukemia inhibitory factor (LIF) were normal. The leukocytes and fibroblasts of all seven newly identified TYK2-deficient patients, unlike those of P1, responded normally to IL-6, possibly accounting for the lack of HIES in these patients. The expression of exogenous wild-type TYK2 or the silencing of endogenous TYK2 did not rescue IL-6 hyporesponsiveness, suggesting that this phenotype was not a consequence of the TYK2 genotype. The core clinical phenotype of TYK2 deficiency is mycobacterial and/or viral infections, caused by impaired responses to IL-12 and IFN-α/β. Moreover, impaired IL-6 responses and HIES do not appear to be intrinsic features of TYK2 deficiency in humans.
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| 3. |
- Schenkel, D., et al.
(författare)
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Linking soil's volatilome to microbes and plant roots highlights the importance of microbes as emitters of belowground volatile signals
- 2019
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Ingår i: Environmental Microbiology. - : Blackwell Publishing Ltd. - 1462-2912 .- 1462-2920. ; 21:9, s. 3313-3327
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Tidskriftsartikel (refereegranskat)abstract
- Plants and microbes release a plethora of volatiles that act as signals in plant–microbe interactions. Characterizing soil's volatilome and microbiome might shed light on the nature of relevant volatile signals and on their emitters. This hypothesis was tested by characterizing plant cover, soil's volatilome, nutrient content and microbiomes in three grasslands of the Swiss Jura Mountains. The fingerprints of soil's volatiles were generated by solid-phase micro-extraction gas chromatography/mass spectrometry, whereas high-throughput sequencing was used to create a snapshot of soil's microbial communities. A high similarity was observed in plant communities of two out of three sites, which was mirrored by the soil's volatilome. Multiple factor analysis evidenced a strong association among soil's volatilome, plant and microbial communities. The proportion of volatiles correlated to single bacterial and fungal taxa was higher than for plants. This suggests that those organisms might be major contributors to the volatilome of grassland soils. These findings illustrate that key volatiles in grassland soils might be emitted by a handful of organisms that include specific plants and microbes. Further work will be needed to unravel the structure of belowground volatiles and understand their implications for plant health and development.
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