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Infection and Immunity, December 1998, p. 5867-5875, Vol. 66, No. 12
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Role of NK Cells in Early Host Response to
Chlamydial Genital Infection
Chien-Te Kent
Tseng, and
Roger G.
Rank*
Department of Microbiology and Immunology,
University of Arkansas for Medical Sciences, Little Rock, Arkansas
72205
Received 13 April 1998/Returned for modification 5 June
1998/Accepted 24 September 1998
The cell-mediated immune response has been documented to be the
major protective immune mechanism in mice infected genitally with the
agent of mouse pneumonitis (MoPn), a biovar of Chlamydia trachomatis. Moreover, there is strong evidence to indicate that gamma interferon (IFN-
) is a major effector mechanism of the cell-mediated immune response. Previous studies from this laboratory have also reported that the dominant cell population in the genital tract is the CD4 Th1 population. When experiments were performed by the
enzyme-linked immunospot assay, high numbers of cells producing IFN-
were found in the genital tract, concomitant with resolution of the
infection; however, in addition, an increase in IFN-
-producing cells
which were CD4
was seen early in the infection. Since
natural killer (NK) cells produce IFN-
and have been found to
participate in the early responses in other infections, we hypothesized
that NK cells are responsible for early IFN-
production in the
murine chlamydial model. NK cells were quantified by the standard YAC-1
cytotoxicity assay and were found to appear in the genital tract as
early as 12 h after intravaginal infection with MoPn. The cells
were confirmed to be NK cells by abrogation of YAC-1 cell cytotoxicity
by treatment in vitro and in vivo with anti-asialo-GM1. The early
IFN-
response could also be depleted by treatment with
anti-asialo-GM1, indicating that NK cells were responsible for the
production of this cytokine. Of interest was our observation that
depletion of NK cells also exacerbated the course of infection in the
mice and elicited a Th2 response, as indicated by a marked increase in
immunoglobulin G1 antibody. Thus, these data demonstrate that NK cells
are not only responsible for the production of IFN-
early in the
course of chlamydial genital tract infection but are also, via IFN-
, a significant factor in the development of the Th1 CD4 response and in
the control of the infection.
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, Mail Slot 511, University of Arkansas for Medical Sciences, Little Rock, AR 72205. Phone: (501) 686-5145. Fax:
(501) 686-5359. E-mail: rankrogerg{at}exchange.uams.edu.
Infection and Immunity, December 1998, p. 5867-5875, Vol. 66, No. 12
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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