|
||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
J. Exp. Med.,
Volume 186, Number 11, December 1, 1997 1843-1851
Receptor
or Immunoglobulin µ Chain Genes
By

From the * Infection and Immunity Group, Department of Biology, National University of Ireland,
Maynooth, County Kildare, Ireland; and the Using a murine respiratory challenge model we have previously demonstrated a role for Th1
cells in natural immunity against Bordetella pertussis, but could not rule out a role for antibody. Here we have demonstrated that B. pertussis respiratory infection of mice with targeted disruptions of the genes for the IFN-
Department of Veterinary Pathology, University College
Dublin, Dublin, Ireland
receptor resulted in an atypical disseminated disease which was
lethal in a proportion of animals, and was characterized by pyogranulomatous inflammation
and postnecrotic scarring in the livers, mesenteric lymph nodes and kidneys. Viable virulent
bacteria were detected in the blood and livers of diseased animals. An examination of the
course of infection in the lung of IFN-
receptor-deficient, IL-4-deficient and wild-type mice
demonstrated that lack of functional IFN-
or IL-4, cytokines that are considered to play major
roles in regulating the development of Th1 and Th2 cells, respectively, did not affect the kinetics
of bacterial elimination from the lung. In contrast, B cell-deficient mice developed a persistent infection and failed to clear the bacteria after aerosol inoculation. These findings demonstrate
an absolute requirement for B cells or their products in the resolution of a primary infection
with B. pertussis, but also define a critical role for IFN-
in containing bacteria to the mucosal
site of infection.
This article has been cited by other articles:
| TABLE OF CONTENTS |
|