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*
Department of Experimental Medicine, Human Anatomy Section, University of Genoa, Genoa, Italy; and
Laboratory of Oncology, Giannina Gaslini Institute, Genoa, Italy
The functional outcome of a T cell response to Ag is the
result of a balance between coactivation and inhibitory signals. In
this study we have investigated the effects of the CD85/leukocyte
Ig-like receptor (LIR)-1/Ig-like transcript (ILT) 2 and of CD152
(CTLA-4) inhibitory receptors on the modulation of cell-mediated immune
responses to specific Ags, both at the effector and at the
resting/memory cell level. Proliferation and cytokine production
of CD4+ T lymphocytes stimulated by recall Ags have been
evaluated. Cross-linking of CD85/LIR-1/ILT2 or CD152 molecules on
cultured T cells using specific mAb and goat anti-mouse antiserum
inhibits Ag-specific T cell proliferation. This inhibition is always
paralleled by increased production of cytokines that down-regulate
immune responses, e.g., IL-10 and TGF-
. In contrast, the
production of cytokines that support T cell expansion and function
(e.g., IL-2, IFN-
, and IL-13) is significantly decreased. A
long-term effect of CD85/LIR-1/ILT2 and of CD152 occurs during
Ag-specific T cell activation and expansion. T cells, primed in the
presence of anti-CD85/LIR-1/ILT2 and anti-CD152 blocking mAb
(but in the absence of cross-linking), proliferate at higher rates and
produce higher amounts of IL-2, IFN-, and IL-13, in comparison with
T cells stimulated with the Ag alone. We also show that the inhibitory
receptors exert a similar effect during Ag activation of specific
CD4+ effector T cells. Ag-specific polyclonal
CD4+ T cell lines exhibit increased proliferation and IL-2,
IFN-, and IL-13 production when the CD85/LIR-1/ILT2 receptor is
blocked by specific mAb. In contrast, cross-linking of this receptor
down-regulates Ag-specific CD4+ T cell proliferation and
increases IL-10 and TGF- production.
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