B cell-deficient mice exposed to schistosoma mansoni develop exacerbated egg pathology which fails to down-modulate during chronic infection

D. Jankovic, M. Kullberp, G. Yap, M. Epstein, A. Cheever, A. Sher

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5 Scopus citations

Abstract

Pathology in schistosome infection is caused by the granulomatous response to parasite eggs deposited in host tissues and the ensuing fibrosis. Previous work established that Th2 CD4+ cells play a major role in expanding granulomatous lesions and in fibrosis in the murine model. To investigate the regulatory role of B lymphocytes in egg induced pathology, B cell-deficient (|iMT) and control C57B1/6 mice were infected with S. mansoni and analyzed at 8 weeks, when granulomas reach maximal size, and at 16 weeks when immune modulation leads to a marked decrease in the volume of these lesions. The number of worm pairs which developed and the number of eggs per worm pair found in tissues were comparable in B cell-deficient and control mice. In contrast, the volume of granulomas was increased significatly by over 60% in B cell-deficient vs. control animals at 8 weeks post infection. Furthermore, the down-modulation of granuloma size evident at 16 weeks in control mice was absent in the B cell-deficient animals. In addition, fibrosis (as measured by tissue collagen) was enhanced in B cell deficient mice both at 8 and 16 weeks. Despite the absence of B cells, the infected |iMT mice were unimpaired in their ability to mount Th2 response to soluble egg Ag. Experiments are in progress to determine if the observed exacerbation in pathology in tMT mice is due to the absence of antibody or another B cell function or product.

Original languageEnglish (US)
Pages (from-to)A1345
JournalFASEB Journal
Volume10
Issue number6
StatePublished - 1996
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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