CD28 signaling in neutrophil induces T-cell chemotactic factor(s) modulating T-cell response

Abstract

We previously reported that human peripheral blood neutrophils express CD28 and interact with macrophage B7 to generate CD28 signaling through PI-3 kinase. Here, we demonstrate that crosslinking of CD28 on neutrophils results in the release of IFN-γ, which restricts amastigote growth and modulates CD4⁺ T cells cytokine secretion. CD28 crosslinking also induces a T-cell chemotactic factor (TCF) that induces chemotactic migration of CD4⁺ T cells. Based on our previous and the current set of data, we propose an operational model explaining how neutrophils are involved in Leishmania infection and how the reported effect of neutrophils on the control of infection is mediated by alteration of T-cell function.