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Infection and Immunity, October 2000, p. 5587-5594, Vol. 68, No. 10
Department of Microbiology and Immunology,
University of Arkansas for Medical Sciences, Little Rock,
Arkansas,1 and Department of Pathology
and Laboratory Medicine, UCLA Medical Center, Los Angeles,
California2
Received 16 March 2000/Returned for modification 3 May
2000/Accepted 7 July 2000
The CD4 T helper cell type 1 (Th1) response is essential for the
resolution of chlamydial genital infection in mice. However, not all
Th1 clones are equally protective in eradicating the infection. Since
oral immunization regimens produce protective immunity, we evaluated
the role of the mucosa-associated homing receptor,
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Expression of Mucosal Homing Receptor
4
7 Is
Associated with Enhanced Migration to the
Chlamydia-Infected Murine Genital Mucosa In
Vivo
4
7, in
trafficking to the genital mucosa. Using a panel of CD4, Th1 cell lines
and clones, we compared the lymphocyte homing patterns of a
Chlamydia-specific, protective clone (P-MoPn), a
nonprotective clone (N-MoPn), and a keyhole limpet hemocyanin
(KLH)-specific cell line (KLH-1). T cells were labeled with the
fluorescent dye PKH-26, adoptively transferred into
Chlamydia-infected mice, and monitored at different time
points throughout the course of a genital infection. We found that
clones P-MoPn and N-MoPn migrated to similar extents to the genital
tract and in significantly greater numbers than the KLH-specific T-cell
line. Both clones and the KLH-1 line expressed similar levels of the
adhesion molecules
4,
1, CD44, and CD11a. However, clones P-MoPn
and N-MoPn expressed higher levels of the mucosal homing receptor,
4
7. Also, clones P-MoPn and N-MoPn but not the KLH-1 line
migrated to the mesenteric lymph node, suggesting a mucosal
recirculation pattern. Moreover, blocking
4
7 adhesion interaction
in vivo significantly reduced the recruitment of P-MoPn but not KLH-1
to the genital tract. These findings show that the mucosal homing
receptor
4
7 is utilized by a subset of CD4 cells during migration
to the Chlamydia-infected genital tract.
*
Corresponding author. Mailing address: UCLA Medical
Center, Department of Pathology and Laboratory Medicine, 10833 Le Conte Ave., Mailroom A2-179 CHS, Los Angeles, CA 90095-1732. Phone: (310)
206-5562. Fax: (310) 794-4863. E-mail:
kkelly{at}mednet.uams.edu.
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