Human disease
IgE responsiveness, atopic
Mondo defines it as: “Immediate hypersensitivity reaction - type I reaction, involves immunoglobulin E (IgE)-mediated release of chemical mediators from mast cells and basophils. Th2 cells produce IL-4 and IL-13, which then act on B cells to promote the production of antigen-specific IgE. Reexposure to the antigen can then result in the antigen binding to and cross-linking the bound IgE antibodies on the mast cells and basophils. This causes the release of preformed mediators (histamine, tryptase, tryptase, chemotactic factors), newly synthesized mediators (leukotrienes, prostaglandin, thromboxane, platelet-activating factor, adenosine, bradykinin), and cytokines from these cells that results in structural and functional changes to the affected tissue.”
1 disease group in OMIA reaches this disease, through OMIA's own Mondo link or its OMIM numbers. The page shows the chain. It does not say whether an animal is a model of this disease.
Animal diseases
By natural-model score for this disease, highest first. The score says how complete and how well supported each chain is, by stated rules. How the score works.
| OMIA group | Name | Found by | Species | The chain reached | Score |
|---|---|---|---|---|---|
| 82 | Atopy | OMIA's OMIM numbers | 2 | Human disease |
12.0
|
Human genes
Each human gene of these disease groups that Open Targets links to this disease.
Open Targets links none of these groups' human genes to this disease.
Drugs tested for this disease
Each ChEMBL drug that has been tested for this disease, and the human genes above it acts on, if any. Open Targets gives some drugs, such as most enzyme replacement therapies, no target gene.
No drug has been tested for this disease.