|
|
||||||||

,
Departments of
*
Immunology and
Laboratory Medicine and Pathology, Mayo Foundation, Rochester, MN 55905; and
Infectious Disease Research Institute and
Corixa Corporation, Seattle Life Sciences Center, Seattle, WA 98104
Infection of different strains of laboratory mice with the agent of
Lyme disease, Borrelia burgdorferi, results in
arthritis, the severity of which has been correlated with the dominance
of Th1 cytokines. In this study, we demonstrate that changes in
B. burgdorferi-specific immunologic responses associated
with pregnancy can alter the outcome of Lyme arthritis in mice. Whereas
nonpregnant female C3H mice consistently developed severe Lyme
arthritis, pregnant mice had a marked reduction in arthritis severity
that was associated with a slight reduction in IFN-
and markedly
increased levels of IL-4 production by B.
burgdorferi-specific T cells. Similar reductions in arthritis
severity and patterns of cytokine production were observed in
nonpregnant, progesterone-implanted mice. Ab neutralization of IL-4 in
progesterone-implanted mice resulted in severe arthritis. Our results
are consistent with the known shift toward Th2 cytokine expression at
the maternal-fetal interface, and are the first to show a
pregnancy-related therapeutic effect in an infectious
model.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |