DiseaseID 27277

哮喘路径

Asthma Pathway

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Disease: 1Symptom: 12Links: 12

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Record Fields

Scalar fields from the final disease record.

Disease Id: 27277
Core Entity Id: 119845
Source Entity Count: 1
Preferred Name: Asthma Pathway
Name Cn: 哮喘路径
Name Pinyin: Xiao Chuan Lu Jing
Name En: Asthma Pathway
Name Latin
Bilingual Status: complete
Disease Type
Umls Disease Type
Disgenet Type
Mesh Class
Do Class
Hpo Class
Mesh Class Name
Hpo Class Name
Do Class Name
Disease Definition: NCI2016_KEGG_1602D:Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into Th2 cells, a process that is promoted by interleukin 4 (IL-4). Activated Th2 cells stimulate B cells to produce IgE antibodies in response to IL-4 and IL-13. IgE binds the high affinity IgE receptor at the surface of mast cells, the proliferation and differentiation of which is promoted by IL-9.The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Activated mast cells and Th2 cells also induce the production of IL-5. IL-5 travels to the bone marrow and regulates the differentiation and egress of eosinophils from the bone marrow into the blood. Moreover activated mast cells and Th2 cells in the lung generate the cytokines interleukin IL-4, IL-13 and tumour necrosis factor (TNF)-alpha. These cytokines stimulate the generation of eotaxin by lung epithelial cells, fibroblasts and smooth muscle cells. Eotaxin then stimulates the selective recruitment of eosinophils from the airway microvessels into the lung tissue. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation.
Version: v2
Suppressed: No

Names

Preferred names, aliases, and source labels retained in the final schema.

Name

Asthma Pathway

Role

preferred

Cross References

Trusted external identifiers retained for this final record.

Umls

C2984299

Sym Map

SMDE06091

Itcmdb Generated

ITX-DISEASE-3AE8737C9ABE

Attributes

Merged source attributes and domain-specific metadata.

Version

Suppress

Disease Definition

NCI2016_KEGG_1602D:Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into Th2 cells, a process that is promoted by interleukin 4 (IL-4). Activated Th2 cells stimulate B cells to produce IgE antibodies in response to IL-4 and IL-13. IgE binds the high affinity IgE receptor at the surface of mast cells, the proliferation and differentiation of which is promoted by IL-9.The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Activated mast cells and Th2 cells also induce the production of IL-5. IL-5 travels to the bone marrow and regulates the differentiation and egress of eosinophils from the bone marrow into the blood. Moreover activated mast cells and Th2 cells in the lung generate the cytokines interleukin IL-4, IL-13 and tumour necrosis factor (TNF)-alpha. These cytokines stimulate the generation of eotaxin by lung epithelial cells, fibroblasts and smooth muscle cells. Eotaxin then stimulates the selective recruitment of eosinophils from the airway microvessels into the lung tissue. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation.