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Infection and Immunity, September 2001, p. 5874-5882, Vol. 69, No. 9
Laboratoire d'Immunopathologie Cellulaire
des Maladies Infectieuses, UMR 8527,1 and
Laboratoire de Synthèse, Structure, et Fonction des
Biomolécules, UMR 8525,2 Institut de
Biologie, F-59021 Lille, France
Received 14 November 2000/Returned for modification 4 January
2001/Accepted 18 May 2001
Genetic factors that might influence susceptibility or resistance
in naive individuals and early-stage pathology in schistosomiasis are
difficult to study in clinical trials, since in areas where the disease
is endemic the first contact with the parasite occurs most often at
very early ages. Therefore, four strains (DR1.A
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.9.5874-5882.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
HLA Class II Polymorphism Influences Onset and
Severity of Pathology in Schistosoma mansoni-Infected
Transgenic Mice
°, DR2.A°,
DQ8.A°, and DQ6.A°) of major histocompatibility complex class
II-deficient mice (A°), transgenic for different HLA alleles, have
been used to evaluate the potential role of HLA class II polymorphism
in the onset of the infection by Schistosoma mansoni. The
survival rates and parasitological and immunological parameters after
infection were evaluated and compared against the control values
obtained with A° mice. All four mouse strains used in this study
were able to generate a specific immune response against S. mansoni antigens (cytokine production and antibody production). However, only mice expressing DR alleles survived until the chronic stage of the infection and were able to mount protective granulomatous response avoiding hepatic damage, presenting predominant gamma interferon production. In contrast, strains expressing DQ alleles revealed an impairment in generating effective granulomas, resulting in
earlier death, which was associated with an impaired hepatic granulomatous response and liquefactic necrosis, reflecting the influence of HLA polymorphism in the establishment of protective response in the early stage of infection.
*
Corresponding author. Mailing address: UMR 8527 CNRS,
Institut de Biologie, 1 rue du Professeur Calmette, BP447, F-59021
Lille, France. Phone: 33 (0) 3-20-87-12-47. Fax: 33 (0) 3-20-87-12-33. E-mail: gerhild.angyalosi{at}ibl.fr.
Infection and Immunity, September 2001, p. 5874-5882, Vol. 69, No. 9
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.9.5874-5882.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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