Previous Article | Next Article ![]()
Infection and Immunity, December 2000, p. 6979-6987, Vol. 68, No. 12
Department of Microbiology, Montana State
University, Bozeman, Montana 59717,1 and
Laboratory of Intracellular Parasites, National Institute of
Allergy and Infectious Diseases, National Institutes of Health,
Rocky Mountain Laboratories, Hamilton, Montana 598402
Received 5 June 2000/Returned for modification 24 August
2000/Accepted 25 September 2000
CD4+ T-helper type 1 (Th1) responses are essential for
the resolution of a primary Chlamydia trachomatis genital
tract infection; however, elements of the immune response that function
in resistance to reinfection are poorly understood. Defining the
mechanisms of immune resistance to reinfection is important because the
elements of protective adaptive immunity are distinguished by
immunological memory and high-affinity antigen recognition, both of
which are crucial to the development of efficacious vaccines. Using in
vivo antibody depletion of CD4+ and CD8+ T
cells prior to secondary intravaginal challenge, we identified lymphocyte populations that functioned in resistance to secondary chlamydial infection of the genital tract. Depletion of either CD4+ or CD8+ T cells in immune wild-type
C57BL/6 mice had a limited effect on resistance to reinfection.
However, depletion of CD4+ T cells, but not
CD8+ T cells, in immune B-cell-deficient mice profoundly
altered the course of secondary infection. CD4-depleted
B-cell-deficient mice were unable to resolve a secondary infection,
shed high levels of infectious chlamydiae, and did not resolve the
infection until 3 to 4 weeks following the discontinuation of anti-CD4
treatment. These findings substantiated a predominant role for
CD4+ T cells in host resistance to chlamydial reinfection
of the female genital tract and demonstrated that CD8+ T
cells are unnecessary for adaptive immune resistance. More importantly,
however, this study establishes a previously unrecognized but very
significant role for B cells in resistance to chlamydial reinfection
and suggests that B cells and CD4+ T cells may function
synergistically in providing immunity in this model of chlamydial
infection. Whether CD4+ T cells and B cells function
independently or dependently is unknown, but definition of those
mechanisms is fundamental to understanding optimum protective immunity
and to the development of highly efficacious immunotherapies against
chlamydial urogenital infections.
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Immunity to Murine Chlamydia trachomatis Genital Tract
Reinfection Involves B Cells and CD4+ T Cells but Not
CD8+ T Cells

*
Corresponding author. Mailing address: Department of
Microbiology, Lewis Hall Room 109, Montana State University, Bozeman, MT 59717. Phone: (406) 994-7959. Fax: (406) 994-4926. E-mail: morrison{at}montana.edu.
Present address: Laboratory of Host Defenses, Tuberculosis Research
Section, National Institute of Allergy and Infectious Diseases,
National Institutes of Health, Rockville, Md.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|