Atopic dermatitis (AD) is a chronic, itching, inflammatory skin disease which is associated with asthma and/or hay fever and a familial occurrence of these conditions. Genetic factors are important in the development of AD, but the exact hereditary pathway is still unknown. Dry skin and the weakened barrier function in patients with AD is very important for the patient's reactions to irritants and other external trigger factors including microorganisms. The standard treatments are topical corticosteroids, topical immunomodulating agents, and emollients. If AD cannot be controlled by this type of treatment, systemic immunomodulating agents may be used. UVB, UVA, or psoralen-UVA may also be used for widespread severe lesions. However, some patients do not respond to these standard treatment, and then it is important to consider the role of microorganisms, house dust mites or food. The role of the Malassezia yeasts in AD, especially AD located to the head and neck region, is now documented in several papers. There are also several papers indicating the role of Candida as an aggravating factor in AD. Patients with AD also develop chronic dermatophyte infections more easily, and patients with AD and chronic dermatophyte infections may show improvement in their AD when treated with antifungal drugs.
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| Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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| Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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| Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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| Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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| Site | Modification | Modifier | Source | Reference |
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| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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| Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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| Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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