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Infection and Immunity, June 2001, p. 3737-3743, Vol. 69, No. 6
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.6.3737-3743.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Gamma Interferon Is Not Required for Arthritis
Resistance in the Murine Lyme Disease Model
Lisa
Glickstein,*
Meg
Edelstein,
and
Jay Zengjun
Dong
Department of Medicine, Division of
Rheumatology/Immunology, New England Medical Center and Tufts
University School of Medicine, Boston, Massachusetts 02111
Received 3 January 2001/Returned for modification 1 March
2001/Accepted 26 March 2001
Lyme arthritis is the most common complication following infection
of human individuals with Borrelia burgdorferi sensu
stricto. In mice, B. burgdorferi infection leads to
arthritis of the tibiotarsal joints. Arthritis severity in mice is
under host genetic control, as BALB/c mice developed mild arthritis but
C3H/He mice developed severe disease following B. burgdorferi infection. To study the role of gamma interferon
(IFN-
) in arthritogenesis, targeted mutant mice lacking the IFN-
receptor (IFN-
R) were infected by inoculation with B. burgdorferi. IFN-
R
/
and parental 129/SvEv mice
developed mild arthritis of similar severity, as determined both by
weekly tibiotarsal joint measurements and histopathology at 2 and 5 weeks postinfection. Both strains of mice had the same spirochetal
burden in the joints, suggesting that the IFN-
R
/
mice were not impaired in controlling spirochetal expansion in vivo.
The wild-type mice mounted a Th1 response, with a predominance of
CD4+ IFN-
+ T cells observed by flow
cytometry. In contrast, the IFN-
R
/
mice mounted a
Th2 response, with a predominance of CD4+ IL-4+
T cells. As expected given their cytokine profile, the
IFN-
R
/
mice produced fewer CD8+
IFN-
+ and MAC-1+ IL-12+ cells
and less immunoglobulin G2a (IgG2a) than their wild-type counterparts.
These results strongly suggest that IFN-
is not required for
arthritis resistance or as part of an effective immune response against
B. burgdorferi.
*
Corresponding author. Mailing address: New England
Medical Center, Division of Rheumatology, Box 406, 750 Washington St., Boston, MA 02111. Phone: (617) 636-8527. Fax: (617) 636-4252. E-mail:
lglickstein{at}lifespan.org.

Present address: Mediplex Rehabilitation Hospital, New Bedford, MA
02745.

Present address: BD PharMingen, San Diego, CA
92121.
Infection and Immunity, June 2001, p. 3737-3743, Vol. 69, No. 6
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.6.3737-3743.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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