A number of epidemiological and clinical studies have suggested an inverse 
association between allergy and helminth infection, such as Schistosomiasis. 
Therefore, we hypothesize that Schistosoma japonicum egg antigens, a type of 
native antigen, can induce production of CD4(+) CD25(+) T cells with regulatory 
activity, modulating airway inflammation and inhibiting asthma development. The 
frequency of CD4(+) CD25(+) T cells was determined by flow cytometry for mice 
treated with ovalbumin (OVA), CD25(+) depletion/OVA, schistosome egg antigens, 
schistosome egg antigens/OVA and for control mice. The ability of CD25(+) T 
cells from these mice to suppress T-cell proliferation and cytokine production 
was investigated both in vivo and in vitro. Results showed that the CD4(+) 
CD25(+) T cells of OVA-treated mice exhibited impaired control of dysregulated 
mucosal T helper 2 responses compared to the controls (P < 0.05). Depletion of 
CD25(+) cells accelerated OVA-induced airway inflammation and increased the 
expression of interleukin (IL)-5 and IL-4. Treatment with schistosome egg 
antigens increased the number and suppressive activity of CD4(+) CD25(+) T 
cells, which made IL-10, but little IL-4. In a murine model of asthma, S. 
japonicum egg antigens decreased the expression of Th2 cytokines, relieved 
antigen-induced airway inflammation, and inhibited asthma development. Thus, we 
provided evidence that S. japonicum egg antigens induced the production of 
CD4(+) CD25(+) T cells, resulting in constitutive immunosuppressive activity and 
inhibition of asthma development. These results reveal a novel form of 
protection against asthma and suggest a mechanistic explanation for the 
protective effect of helminth infection on the development of allergy.