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Secretion and Restriction of Leishmania Growth1
* National Center for Cell Science, Ganeshkhind, India; and
Department of Life Science and Biotechnology, Jadavpur University, Calcutta, India
We previously showed that CD28 is expressed on human peripheral
blood neutrophils and plays an important role in CXCR-1 expression and
IL-8-induced neutrophil migration. In this work we demonstrate that
Leishmania major infection of macrophages results in
parasite dose-dependent IL-8 secretion in vitro and in IL-8-directed
neutrophil migration, as blocked by both anti-IL-8 and
anti-IL-8R Abs, toward the L. major-infected
macrophages. In the neutrophil-macrophage cocultures, both CTLA4-Ig, a
fusion protein that blocks CD28-CD80/CD86 interaction, and a
neutralizing anti-IFN-
Ab inhibit the anti-leishmanial
function of neutrophils, suggesting that the neutrophil-macrophage
interaction via CD28-CD80/CD86 plays an important role in the
IFN--dependent restriction of the parasite growth. Cross-linking of
neutrophil-expressed CD28 by monoclonal anti-CD28 Ab or B7.1-Ig or
B7.2-Ig results in phosphatidylinositol 3-kinase association with CD28
and in wortmannin-sensitive but cyclosporin A-resistant induction and
secretion of IFN-. Whereas the neutrophils secrete IFN- with CD28
signal alone, the T cells do not secrete the cytokine in detectable
amounts with the same signal. Thus, neutrophil-expressed CD28 modulates
not only the granulocyte migration but also induction and secretion of
IFN- at the site of infection where it migrates from the
circulation.
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