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Infection and Immunity, March 2000, p. 1428-1434, Vol. 68, No. 3
Department of Pathobiology, School of
Veterinary Medicine, University of Pennsylvania, Philadelphia,
Pennsylvania 19104
Received 19 July 1999/Returned for modification 3 September
1999/Accepted 8 December 1999
The ability to activate macrophages in vitro for nitric oxide
production and killing of Leishmania major parasites is
dependent on tumor necrosis factor, although L. major-infected mice lacking the TNF receptor p55
(TNFRp55
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Activated T Cells Induce Macrophages To Produce NO
and Control Leishmania major in the Absence of Tumor
Necrosis Factor Receptor p55
/ mice) or both the TNFRp55 and TNFRp75
(TNFRp55p75/ mice) are able to produce NO in vivo and
eliminate the parasites. Here we report that activated T cells
cocultured with macrophages results in TNFR-independent activation
sufficient to control parasites and that both CD40/CD40L and LFA-1
contribute to T-cell-mediated macrophage activation. Thus,
anti-CD3-stimulated T cells activated TNFR-deficient macrophages, while
T cells from CD40L/ mice were partially defective in
triggering NO production by TNFRp55p75/ macrophages.
Moreover, in the presence of gamma interferon, anti-CD40 monoclonal
antibody (MAb) activated TNFR-deficient macrophages. Finally, MAb
blockade of LFA-1 completely inhibited macrophage NO production. Our
data indicate that T cells can activate macrophages in the absence of
TNF, thus providing a mechanism for how TNFR-deficient mice can control
intracellular pathogens.
*
Corresponding author. Mailing address: Department of
Pathobiology, School of Veterinary Medicine, University of
Pennsylvania, 3800 Spruce St., Philadelphia, PA 19104. Phone: (215)
898-1602. Fax: (215) 573-7023. E-mail:
pscott{at}vet.upenn.edu.
Infection and Immunity, March 2000, p. 1428-1434, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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