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IL-13 Acutely Augments HIV-Specific and Recall Responses from HIV-1-Infected Subjects In Vitro by Modulating Monocytes¹

Emmanouil Papasavvas^*, Junwei Sun^*, Qi Luo^*, Elizabeth C. Moore^*, Brian Thiel^*, Rob Roy MacGregor, Adrian Minty, Karam Mounzer, Jay R. Kostman^, and Luis J. Montaner^2,*

^* The Wistar Institute, Philadelphia, PA 19104; Infectious Diseases Division, University of Pennsylvania, Philadelphia, PA 19104; Molecular and Functional Genomics Department, Sanofi-Synthelabo Recherche, Labege, France; and Philadelphia Field Initiating Group for HIV-1 Trials, Philadelphia, PA 19107

We show in this study that acute exposure of PBMCs derived from HIV-infected subjects to IL-13 results in increased recall T cell lymphoproliferative responses against HIV-1 p24 (n = 30, p < 0.0001) and other recall Ags (influenza, n = 43, p < 0.0001; purified protein derivative tuberculin, n = 6, p = 0.0299). This effect is due to a mechanism that acutely targets APC function in the adherent monocyte subset, as shown by the expansion of CD4⁺ T cell responses following coculture of IL-13-treated enriched CD14⁺ monocytes with donor-matched enriched CD4⁺ T cells and Ag. Exposure to IL-13 over 18–72 h resulted in a significant enhancement of monocyte endocytosis (n = 11, p = 0.0005), CD86 expression (n = 12, p = 0.001), and a significant decrease in spontaneous apoptosis (n = 8, p = 0.008). Moreover, IL-13 exposure induced a significant decrease of significantly elevated constitutive levels of PBMC-secreted TNF- (n = 14, p < 0.001) and IL-10 (n = 29, p < 0.001) within 18 h of exposure ex vivo, also reflected by decreased gene expression in the adherent cell population. Our data show that IL-13 is able to acutely enhance the function of the CD14⁺ cell subset toward supporting Ag-specific cell-mediated responses in chronic HIV-1 infection.