Abstract
Groups of progesterone-treated female CBA/nu mice were adoptively transferred with immune spleen cells or pooled antisera from congenic immunocompetent CBA donors that had been infected with a 'fast', human strain (SA-2f) of Chlamydia trachomatis. The spleen cells were given either intravenously (6.3 X 10(7) cells) or intraperitoneally (9.5 X 10(7) cells), and the antiserum (antibody titre 1:4096) was given intravenously. Strain SA-2f was introduced into the uterine cavity of these mice approximately 3 h after cell or antiserum transfer; antiserum was given also at intervals up to 23 days later. Untreated mice serving as controls were inoculated with chlamydiae in the same way. Subsequent recovery of chlamydiae from mice in the various groups indicated that transfer of cells or antiserum had not abrogated the chlamydial infections, despite high titres of chlamydial IgG antibody in the sera of all the recipient mice. These results confirm our earlier findings but are unlike those of some other investigators working with different mouse model systems. It seems that there are differences between systemic/respiratory immune mechanisms and those which operate locally in the uterus, which may be regarded as an immunologically privileged site.
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