Premium
Correlations between worm burden and markers of Th1 and Th2 cell subset induction in an inbred strain of mouse infected with Trichuris muris
Author(s) -
Else K.J.,
Entwistle G.M.,
Grencis R.K.
Publication year - 1993
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.1993.15.10.595
Subject(s) - biology , immunology , trichuriasis , trichuris , serology , parasite hosting , inbred strain , t cell , immunoglobulin e , immune system , eosinophilia , helminths , antibody , ascariasis , genetics , world wide web , computer science , gene
Summary Helper T cell subset induction was examined within a single inbred strain of mouse ( B10.D2/n) where individuals varied in their ability to expel the nematode parasite Trichuris muris . In this mouse strain approximately half of infected individuals resist infection whilst half are unable to expel the parasite and harbour chronic mature adult worm infections. We here assess various T cell and serological parameters in individual B10.D2/n mice infected with T. muris in relation to the number of parasites harboured. Worm burdens showed very significant negative correlations with five different parameters indicative of the selective expansion within the host of helper T cells of the Th2 subset. Thus, in vitro IL‐5 and 1L‐9 production by restimulated mesenteric lymph node cells, totallgE levels, the early parasite‐specific IgG1 response (all P < 0·01) and intestinal eosinophilia ( P < 0·05), were all significantly negatively correlated with worm burden. In addition, levels of IL‐3 were significantly greater in mice resistant to infection ( P < 0·01). In contrast there was a significant positive correlation between worm burden and parasite‐specific IgG2a levels ( P < 0·05), IgG2a production being under the tight control of the Th1‐specific cytokine IFN‐y and thus a reliable marker for in vivo Th1 cell activation. The data demonstrates that an individual infected with T. muris is capable of mounting either a protective Th2‐type response or an inappropriate Th1‐type response. Thus, under conditions where host genetic factors and route of antigen introduction into the host are identical, polarized helper T cell responses can arise and hence may be due to a parasite‐derived influence rather than an intrinsic difference between hosts per se.