An early intestinal mucosal source of gamma interferon is associated with resistance to and control of Cryptosporidium parvum infection in mice

Infect Immun. 2005 Dec;73(12):8425-8. doi: 10.1128/IAI.73.12.8425-8428.2005.

Abstract

Resistance to and control of Cryptosporidium parvum infection in mice in the absence of adaptive immunity appears to be gamma interferon (IFN-gamma) dependent. Using an IFN-gamma-neutralizing antibody in a murine model, we demonstrated increased susceptibility to infection within 24 h. We correlated this early resistance and control with increased mucosal expression of IFN-gamma and demonstrate that CD8+ T-cell receptor alphabeta intestinal intraepithelial lymphocytes express and secrete this cytokine shortly after infection. The rapid kinetics of IFN-gamma expression and secretion by naive CD8+ T cells in response to a protozoan pathogen have not previously been demonstrated.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies / pharmacology
  • Antigens, Protozoan / immunology
  • CD8-Positive T-Lymphocytes / immunology*
  • Cryptosporidiosis / immunology*
  • Cryptosporidium parvum*
  • Disease Susceptibility
  • Interferon-gamma / antagonists & inhibitors
  • Interferon-gamma / metabolism*
  • Intestinal Mucosa / immunology*
  • Intestinal Mucosa / parasitology
  • Intestinal Mucosa / pathology
  • Intestine, Small / immunology
  • Intestine, Small / pathology
  • Mice
  • Receptors, Antigen, T-Cell, alpha-beta / analysis

Substances

  • Antibodies
  • Antigens, Protozoan
  • Receptors, Antigen, T-Cell, alpha-beta
  • Interferon-gamma