No abstract

Antigenic proteins were characterized by the immunoblotting technique with sera from rats and mice after infection as well as hyperimmune sera. The immune response of infected animals was mainly directed toward five proteins of adult worms (190, 118, 110, 98, and 52 kDa) and four proteins of the third larval stage (L3; 92, 78, 58, and 24 kDa). The immunoblots indicated that stage-specific proteins of the homogenates were recognized. Three stage-specific proteins of L3 larvae (150, 135, and 125 kDa) and three proteins typical to the adult worm (100, 82, and 67 kDa) were identified. The majority of the worm proteins elicited an IgG response. IgE synthesis was induced by living and dead parasites and was directed towards four proteins (190, 150, 125, and 98 kDa). Three proteins additionally induced an IgG or IgM antibody response. The immune response as shown by the immunoblotting technique seems to be directed towards (1) antigens that are present for the duration of an infection and (2) stage-specific antigens that are expressed for only a short time during the life cycle of the parasite.

In vitro IgE synthesis by lymphoid cells was studied during the course of infection of mice with Nippostrongylus brasiliensis. The studies involved inbred strains of mice which had been shown to be high IgE responders (A.CA, B10.M), or non-responders (Balb/c, B10.D2) to parasite antigen. In addition, F1 hybrids of low and high responders and irradiated non-responders were studied. Infection with N. brasiliensis led to an increase in IgE synthesis in vitro which was most pronounced during reinfection of mice. Addition of mitogens e.g. pokeweed mitogen (PWM), lipopolysaccharide (LPS), concanavalin A (ConA) to the cultures induced enhancement, suppression or had no effect on IgE synthesis. Addition of N. brasiliensis homogenate or worm culture supernatant led to a fluctuating pattern of IgE synthesis. No correlation was found between lymphocyte proliferative response to mitogen and worm antigens and IgE synthesis. Our data suggest, that PWM is more likely to enhance IgE synthesis in vitro than LPS or ConA. An enhancement is more easily observed with the cells of non-infected animals or during the early phase of infection or reinfection. The mitogen-induced increase in IgE synthesis did not exceed the values obtained during infection or reinfection.

We investigated the IgE-antibody response in 36 inbred mouse strains during infection with Nippostrongylus brasiliensis. With regard to the N. brasiliensis-specific IgE-antibody activity responder and nonresponder mice were obtained. Mice with the H-2-f haplotype (A.CA, B10.M, A.TFR 5) are high specific responded. It is suggested that one Ir gene for the N. brasiliensis-induced IgE-antibody response is localized within the K to J region of the mouse major histocompatibility complex. To obtain a medium IgE-antibody response it appears that a complementation between two Ir genes is necessary. An additional genetic control beyond the H-2 complex cannot be excluded. As to the total nonspecific serum IgE levels the parasitic infection leads to a 20- to 40-fold increase in high and low specific responder strains as well. Pretreatment of high responder mice (A.TFR 5, B10.M) with sera that were obtained from normal or complete Freund’s adjuvant treated low (B10.G) and nonresponder (A.TFR 1) mice led to significant inhibition or enhancement of the N. brasiliensis-specific IgE-antibody response.

No abstract