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CUTTING EDGE |
*
Infectious Disease Research Institute and
Corixa Corp., Seattle, WA 98104;
Department of Microbiology, University of Western Australia, Nedlands, Australia;
§
Department of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil; and
¶
Immunex Corp., Seattle, WA 98101
It has been proposed that the induction of cellular immunity and
resistance to intracellular pathogens is dependent upon CD40 ligand
(CD40L). In the present study we show that this proposal is not
ubiquitously supported. Mice genetically deficient in CD40L (CD40LKO)
were resistant to i.v. infection with Mycobacterium
tuberculosis when assessed by survival and bacteriologic burden
in the spleen, liver, and lungs. Infected CD40LKO mice developed
granulomas that lacked epithelioid cells and were less numerous and
markedly smaller than those observed in control mice. Upon stimulation
with purified protein derivative of M. tuberculosis,CD4+ T cells from infected CD40LKO mice proliferated
and produced high levels of IFN-
but not IL-4. Finally, spleen cells
from CD40LKO mice stimulated with M. tuberculosis produced
IL-12, TNF, and nitric oxide levels comparable to those produced by
control cells. In contrast to original proposals, these data clearly
show that protective Th1 immunity can be achieved against intracellular
pathogens (e.g., Mycobacterium) independently of
CD40L.
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