Infection of mice lacking interleukin-7 (IL-7) reveals an unexpected role for IL-7 in the development of the parasite Schistosoma mansoni.

Abstract:

:A single intradermal administration of recombinant interleukin-7 (IL-7) has been shown to aggravate the course of murine schistosomiasis, to favor the development of Th2-associated antibodies specific for the parasite, and to alter migration kinetics and/or migratory route of the parasite within its vertebrate host. Here we show that after infection of IL-7-deficient mice with Schistosoma mansoni, the predominant parasite-specific humoral response follows a Th1 pattern, and the development of the parasite is greatly impaired. In IL-7-deficient mice, increased numbers of larvae reach the lungs and fewer larvae reach the liver, compared to control mice. In the absence of IL-7, female worms show an altered fecundity, leading to decreased numbers of eggs trapped in the tissues and to an amelioration of the pathology of the infected host. The most striking observation is the blockade of parasite growth in an IL-7-defective environment, leading to dwarf male and female worms. The results of this study have important implications for the role of IL-7 in the host-parasite relationship and show how parasites can disable or evade the host immune response.

journal_name

Infect Immun

journal_title

Infection and immunity

authors

Wolowczuk I,Nutten S,Roye O,Delacre M,Capron M,Murray RM,Trottein F,Auriault C

doi

10.1128/IAI.67.8.4183-4190.1999

keywords:

subject

Has Abstract

pub_date

1999-08-01 00:00:00

pages

4183-90

issue

8

eissn

0019-9567

issn

1098-5522

journal_volume

67

pub_type

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