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and IL-12 Production by Monocytes and Dendritic Cells1
*
Laboratoire de Recherche sur l’Allergie, Université de Montréal, Centre de Recherche Louis-Charles Simard, Montréal, Québec, Canada; and
Unité d’Immunologie Cellulaire, Institut Gustave-Roussy, Villejuif, France
Lymphocyte activation gene-3 (LAG-3) is an MHC class II ligand
structurally and genetically related to CD4. Although its expression is
restricted to activated T cells and NK cells, the functions of LAG-3
remain to be elucidated. Here, we report on the expression and function
of LAG-3 on proinflammatory bystander T cells that are activated in the
absence of TCR engagement. LAG-3 is expressed at high levels on human T
cells cocultured with autologous monocytes and IL-2 and synergizes with
the low levels of CD40 ligand (CD40L) expressed on these cells to
trigger TNF-
and IL-12 production by monocytes. Indeed,
anti-LAG-3 mAb inhibits both IL-12 and IFN-
production in
IL-2-stimulated cocultures of T cells and autologous monocytes. Soluble
LAG-3Ig fusion protein markedly enhances IL-12 production by monocytes
stimulated with infra-optimal concentrations of sCD40L, whereas it
directly stimulates monocyte-derived dendritic cells (DC) for the
production of TNF- and IL-12, unravelling an enhanced responsiveness
to MHC class II engagemenent in DC as compared with activated
monocytes. Thus similar to CD40L, LAG-3 may be involved in the
proinflammatory activity of cytokine-activated bystander T cells and
most importantly it may directly activate DC.
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