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*
Immunology Unit, Glaxo Wellcome Medicines Research Centre, Stevenage, United Kingdom; and
Edward Jenner Institute for Vaccine Research, Compton, Berkshire, United Kingdom
L-selectin has become established as a key molecule in the
recirculation of naïve T cells from the blood to peripheral
lymph nodes, yet little is known about its role in the migration of
effector or memory cells. While differentiating naïve
CD4+ T cells into Th1 and Th2 subsets in vitro, it was
noted that L-selectin levels were maintained on the Th1 subset of
cells. The expression of L-selectin on the Th1 cells appeared to be
dependent on the presence of IL-12. Th2 cells, differentiated in the
absence of IL-12, failed to maintain L-selectin expression. Coculture
with IL-12, IL-18, IL-4, TNF-
, or IFN-, -
, or -
demonstrated a dependence on IL-12 alone for L-selectin expression. In
addition, the inclusion of heat-killed Listeria
monocytogenes in the cultures also maintained L-selectin
expression on the Th1 cells. In all cultures, the maintenance of
L-selectin on the T cell surface could be blocked by the inclusion of
anti-IL-12 Abs. Analysis of the mRNA levels for L-selectin in T
cells, differentiated in the presence or absence of IL-12, showed that
the cytokine appears to exert its effect on L-selectin at the
transcriptional level. Given the key role played by IL-12 in the
differentiation of naïve T cells into the Th1 subset, the
observation that IL-12 can also regulate L-selectin expression has
implications for the migration of Th1 effector cells both through the
lymphatic system and to sites of inflammation.
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