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Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104
Infection with Leishmania major in BALB/c mice is
accompanied by the development of a nonprotective Th2-type response. It
has previously been shown that disease progression, and the activation
of a Th2-type response, can occur in the absence of CD28 costimulation
following the inoculation of high numbers of L. major
promastigotes. In this study, we show that in the absence of CD28-B7
interactions, BALB/c mice can spontaneously resolve their infections
following the inoculation of low numbers of parasites. BALB/c
CD28+/+ and CD28-/- mice were inoculated with
250, 500, and 750 metacyclic parasites. The CD28-/- mice
controlled their lesions, whereas the wild-type (WT) mice developed
progressive nonhealing infections. Resistance to infection was
associated with reduced numbers of parasites in the
CD28-/- mice compared with the WT mice. Infection of the
CD28-/- mice resulted in the activation of a Th1-type
response as evidenced by increased levels of mRNA for IFN-
and
reduced levels of message for IL-4 and IL-10 in draining lymph
nodes compared with those in WT mice. Healing of infected
CD28-/- mice could also be ablated with anti-CD4 Ab
treatment or treatment with anti-IFN- Ab. In addition, healed
CD28-/- mice were resistant to a challenge infection with
L. major. These results suggest that CD28 costimulation
influences the in vivo activation of a Th2-type response in a manner
that is dependent on the size of the parasite
inoculum.
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