Previous Article | Next Article ![]()
Infection and Immunity, November 1998, p. 5208-5214, Vol. 66, No. 11
Department of Medicine and Gwen Knapp Center
for Lupus and Immunology Research, Committee on Immunology,
University of Chicago, Chicago, Illinois 60637
Received 4 March 1998/Returned for modification 5 May 1998/Accepted 3 August 1998
Infection of susceptible mouse strains with Borrelia
burgdorferi, the agent of Lyme disease, results in the
development of arthritis. Components of the innate immune
system may be important mediators of this pathology. To investigate the
potential role of NK cells in development of experimental Lyme
arthritis, we examined their activation in vivo in both resistant and
susceptible mouse strains. Following inoculation of B. burgdorferi into the footpad, lymph node NK cells from
susceptible C3H/HeJ (C3H) mice produced more gamma interferon than NK
cells from resistant DBA/2J mice. Lymph node cells from susceptible C3H
and AKR mice also had increased ability to lyse YAC-1 target cells 2 days following infection. Antibody depletion of NK cells from
susceptible mice, however, did not alter the development of arthritis
following B. burgdorferi challenge. In addition, NK cell
depletion had little effect on spirochete burden. Thus, there is a
marked activation of NK cells in susceptible mouse
strains following infection. Although NK cells are not absolutely
required for arthritis, events occurring prior to NK cell activation
might be important in mediating pathology in experimental Lyme disease.
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Activation of Natural Killer Cells in Arthritis-Susceptible but
Not Arthritis-Resistant Mouse Strains following Borrelia
burgdorferi Infection
*
Corresponding author. Mailing address: Gwen Knapp
Center for Lupus and Immunology Research, University of Chicago, 924 E. 57th St., Chicago, IL 60637. Phone: (773) 702-4730. Fax: (773) 702-1576. E-mail: sreiner{at}midway.uchicago.edu.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»