RGD Reference Report - Cutting edge: the absence of C3 demonstrates a role for complement in Th2 effector functions in a murine model of pulmonary allergy. - Rat Genome Database

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Cutting edge: the absence of C3 demonstrates a role for complement in Th2 effector functions in a murine model of pulmonary allergy.

Authors: Drouin, SM  Corry, DB  Kildsgaard, J  Wetsel, RA 
Citation: Drouin SM, etal., J Immunol. 2001 Oct 15;167(8):4141-5.
RGD ID: 5129517
Pubmed: PMID:11591733   (View Abstract at PubMed)

Asthma is a chronic disease of the lung resulting from airway obstruction. Although the initiating causes are not entirely clear, the airway inflammation in asthma is associated with Th2 lymphocytes and their cytokines, particularly IL-4, which play a prominent role in this disease by regulating airway hyperresponsiveness, eosinophil activation, and IgE synthesis. Historically, complement was not thought to contribute to the pathogenesis of asthma. However, using C3-deficient mice in an allergen-induced model of pulmonary allergy, we demonstrate that complement may impact key features of this disease. When challenged with allergen, mice deficient in C3 exhibit diminished airway hyperresponsiveness and lung eosinophilia. Furthermore, these mice also have dramatically reduced numbers of IL-4-producing cells and attenuated Ag-specific IgE and IgG1 responses. Collectively, these results demonstrate that C3-deficient mice have significantly altered allergic lung responses and indicate a role for the complement system in promoting Th2 effector functions in asthma.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
asthma  ISOC3 (Mus musculus)5129517; 5129517 RGD 
asthma  IMP 5129517 RGD 

Objects Annotated

Genes (Rattus norvegicus)
C3  (complement C3)

Genes (Mus musculus)
C3  (complement component 3)

Genes (Homo sapiens)
C3  (complement C3)


Additional Information