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Blood, Vol. 93 No. 4 (February 15), 1999:
pp. 1277-1286
CD8 T-Cell Infiltration in Extravascular Tissues of Patients With
Human Immunodeficiency Virus Infection. Interleukin-15 Upmodulates
Costimulatory Pathways Involved in the Antigen-Presenting Cells-T-Cell
Interaction
Carlo Agostini,
Renato Zambello,
Monica Facco,
Alessandra Perin,
Francesco Piazza,
Marta Siviero,
Umberto Basso,
Michela Bortolin,
Livio Trentin, and
Gianpietro Semenzato
From Padua University School of Medicine, Department of Clinical and
Experimental Medicine, Padua Hospital, Padua, Italy.
Interleukin (IL)-15 regulates the proliferative activity of the
CD8+ T-cell pool in human immunodeficiency virus
(HIV)-infected patients, thereby contributing to the maintenance of the
CD8+ T-cell-mediated immune response against HIV in
extravascular tissues, including the lung. However, the effects of
IL-15 on antigen-presenting cells (APC) during HIV infection are still unclear. In this study, we evaluated whether IL-15 regulates the macrophage stimulatory pathways governing inflammatory events that take
place in the lung of patients with HIV infection. As a first step we
evaluated the in vitro effects of IL-15 on lung macrophages retrieved
from the respiratory tract of eight normal subjects. Although
macrophages from uninfected individuals expressed the IL-15 binding
proteins (IL-15R and the common  c) at resting conditions, they
did not express IL-15 messenger RNA (mRNA). However, a 24-hour
stimulation with IL-15 induced the expression of interferon- (IFN-) and IL-15 itself, suggesting a role for this cytokine in the
activation of the pulmonary macrophage pool during inflammation. As a
confirmation of the role of IL-15 in this setting, at resting conditions, alveolar macrophages of patients with HIV infection and
T-cell alveolitis expressed IL-15, IFN-, and IL-15 binding proteins;
showed an upmodulation of costimulatory molecules, B7 and CD72, which
are involved in the APC of macrophages; and behaved as effective
accessory cells because they elicited a strong proliferation of T
cells. The accessory effect was inhibited by pretreatment with
anti-CD72, anti-B7 (CD80 and CD86), and anti-IL-15 monoclonal antibodies (MoAb). We then investigated the relationship between IL-15
and the expression of costimulatory molecules by macrophages. A 24-hour
stimulation of IL-15R+/c+ macrophages
with IL-15 upregulated the expression of CD80 and CD86. The evidence
that IL-15 upregulates the expression of coligands that favor the
contact between T cells and APC, per se, triggers T-cell activation and
proliferation and acts as a chemoattractant for T cells, suggests that
IL-15 plays a key role in Tc1-mediated defense mechanisms taking place
in extravascular tissues of patients with HIV disease.
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