Elevated serum lgE and pheripheral blood eosinophilia are immunologic hallmark in helminthic infections. Recently, these responses are known to be regulated by Th2-specific cytokine IL-4 and IL-5, respectively. And also, the antagonistic effects of IFN-γ on Th2 cell proliferation were shown in vitro. However, few studies on the effect of IFN-γ on Th2 cytokine responses in Paragonimus westermani infection are reported, In this study, effects of rIFN-γ on serum lgE production and the number of pheripheral blood eosinophils in mice infected with P.westermani were examined.

5-6week old male BALB/c mice treated with IFN-γ were divided into 3 groups. All the mice were inoculated orally with 20 metacercariae of P.westermani. GroupImice(0-14days) were treated intraperitoneally with 2×10³ unit of rIFN-γ at daily intervals from the time of the infection to 4th day infection, group II mice(5-14 days) were treated with rIFN-γ from the 5th to the 14th day of infection and group III mice(8-14 days) were treated from the 8th to the 14th of infection. Total serum lgE and the number of pheripheral blood eosinophils were examined in infected mice treated with rIFN-γ.

The serum lgE levels in groupIand II were decreased compared with those of infected mice with no treatment with rIFN-γ, but not significantly. The number of pheripheral blood eosinophils in group I and II were decreased compared with those of infected mice with no treatment with rIFN-γ, especially significant(p<0.05) reduction was shown in group I. However, the serum lgE levels and number of pheripheral blood eosinophils in group III were similar to those of infected mice with no treatment with rIFN-γ.

These results suggest that IFN-γ decreases Th2 cytokine response in P.westermani-infected mice. However, IFN-γ treatment has less of an effect once the production of Th2-associated cytokines has become established.

Elevation of serum lgE is the most characteristic immune response in helminthic infections. Recently, expression of CD23(FcεRII on B lymphocytes play a major role in lgE production in allergic diseases. However, the mechanisms causing increased lgE production during helminthic infections are poorly understood. In the present study, the expression of CD 23 on splenic B lymphocytes during the course of infection with Paragonimus westermani was examined.

Female, 4-6-week old BALB/c mice were inoculated orally with 20 metacercariae of P. westermani. For detection of CD23 positive B lymphocytes by flow cytometry, splenocytes from infected mice and non-infected age matched controls were stained with FITC-conjugatedrat anti-mouse DB23 and PE-conjugated rat anti-mouse CD45R/B220 mono-clonal antibody. And also, to observe the effect of metacercarial ESP on the expression of CD23 antigen, splenocytes from non-infected mice were incubated in the presence of ESP at 37℃ for 6 h and 24 h.

The frequency of CD23 positive B lymphocytes of infected mice was increased significantly(p<0.05) at two and three weeks after infection(43.4±7.52% and 44.4±2.99%, respectively) and persisted the higher levels at four and six weeks after infection. Expression of CD23 antigen of cultured splenocytes from non-infected mice in the presence of metacercarial ESP was increased significantly(p<0.05) at 24 h after incubation(60.1±7.54%).

These results suggest that the expression of CD23 antigen induced by metacercarial ESP might play a important role in serum lgE production in mice infected with P. westermani.