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Departments of
*
Immunology and
Urology, Cleveland Clinic Foundation, Cleveland, OH 44195;
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106; and
§
¶
Immunology Department, Pfizer, Inc., Groton, CT 06340
Recent studies have suggested a pivotal role for secondary lymphoid
chemokine (SLC) in directing dendritic cell trafficking from peripheral
to lymphoid tissues. As an extension of these studies, we examined the
consequences of anti-SLC Ab treatment during Ag priming on T cell
function in an inflammatory response. We used a model of T
cell-mediated inflammation, contact hypersensitivity (CHS), where
priming of the effector T cells is dependent upon epidermal dendritic
cell, Langerhans cells, and migration from the hapten sensitization
site in the skin to draining lymph nodes. A single injection of
anti-SLC Ab given at the time of sensitization with FITC inhibited
Langerhans cell migration into draining lymph nodes for at least 3
days. The CHS response to hapten challenge was inhibited by
anti-SLC Ab treatment in a dose-dependent manner. Despite the
inhibition of CHS, T cells producing IFN-
following in vitro
stimulation with anti-CD3 mAb or with hapten-labeled cells were
present in the skin-draining lymph nodes of mice treated with
anti-SLC Ab during hapten sensitization. These T cells were unable,
however, to passively transfer CHS to naive recipients. Animals treated
with anti-SLC Ab during hapten sensitization were not tolerant to
subsequent sensitization and challenge with the hapten. In addition,
anti-SLC Ab did not inhibit CHS responses when given at the time of
hapten challenge. These results indicate an important role for SLC
during sensitization for CHS and suggest a strategy to circumvent
functional T cell priming for inflammatory responses through
administration of an Ab inhibiting dendritic cell
trafficking.
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