HUMAN-IMMUNOGLOBULIN-E RESPONSES TO A RECOMBINANT 22.6-KILODALTON ANTIGEN FROM SCHISTOSOMA-MANSONI ADULT WORMS ARE ASSOCIATED WITH LOW INTENSITIES OF REINFECTION AFTER TREATMENT
M. Webster et al., HUMAN-IMMUNOGLOBULIN-E RESPONSES TO A RECOMBINANT 22.6-KILODALTON ANTIGEN FROM SCHISTOSOMA-MANSONI ADULT WORMS ARE ASSOCIATED WITH LOW INTENSITIES OF REINFECTION AFTER TREATMENT, Infection and immunity, 64(10), 1996, pp. 4042-4046
Schistosoma mansoni-infected individuals who have low intensities of r
einfection following treatment produce immunoglobulin E (IgE) antibodi
es against a range of S. mansoni adult-worm antigens. One of the targe
ts of the IgE response is an adult-worm sodium dodecyl sulfate-polyacr
ylamide gel electrophoresis band of 22 kDa (Sm22), which contains an a
ntigen(s) located within the tegument and gut lining of adult worms an
d relatively late schistosomula life cycle stages only. A significant
negative correlation between the level of anti-Sm22 IgE and the intens
ity of reinfection following treatment suggests that IgE responses aga
inst this antigen(s) are characteristic of individuals who are resista
nt to reinfection. To identify the antigen(s) in the Sm22 band that ar
e associated with these IgE responses, we have cloned and characterize
d a recombinant 22-kDa protein (rSm22) that cross-reacts immunological
ly with Sm22. There was a high correlation between native and recombin
ant Sm22 isotype responses, indicating that the correct antigen had be
en cloned and that responses against rSm22 made up the majority of the
responses against Sm22. By analyzing human isotype responses to rSm22
with human sera from a longitudinal treatment and reinfection study a
nd correlating the anti-rSm22 isotype responses, retrospectively, with
the intensity of reinfection following treatment for each individual,
we observed a negative correlation between the IgE response to rSm22
and the intensity of reinfection. This relationship remained significa
nt after allowing for age and other isotype responses to rSm22, in par
ticular IgG4.