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Rocky Mountain Laboratories, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Hamilton, MT 59840
Immunity to genital tract infection with Chlamydia
trachomatis is mediated by type 1 CD4+ T
lymphocytes. To define the signals that govern lymphocyte trafficking
to the genital mucosa, integrins expressed by infiltrating T cells and
endothelial addressins displayed on local vasculature were
characterized during the course of infection. All T cells expressed the
Lß2 heterodimer that binds vascular
ICAM-1, and most displayed enhanced levels of the
4ß1 integrin that interacts with VCAM-1.
E and ß7low integrin chains
were detected on approximately 15 and 30% of infiltrating T cells,
respectively. Lymphocytes derived from the spleen or draining lymph
nodes expressed this same integrin profile, suggesting that cells are
recruited to the genital mucosa from the systemic circulation without
significant selection pressure for these markers. Immunofluorescent
staining for the corresponding vascular addressins revealed intense
expression of VCAM-1 on small vessels within
Chlamydia-infected genital tracts and up-regulation of
ICAM-1 on endothelial, stromal, and epithelial cells. Mucosal addressin
cell adhesion molecule-1 was not detected within genital tissues. These
results indicate that T lymphocyte homing to the genital mucosa
requires the interaction of Lß2 and
4ß1 with endothelial ICAM-1 and VCAM-1,
respectively, which is the same pathway that directs lymphocytes to
systemic sites of inflammation. Homing pathways defined for the
intestinal mucosa and assumed to be relevant to all mucosal sites are
not well represented in the genital tract. The identification of T
lymphocyte trafficking pathways shared between systemic and mucosal
tissues should facilitate vaccine strategies aimed at maximizing immune
responses against Chlamydia and other pathogens of the
urogenital tract.
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