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Regulates Corneal Langerhans Cell Migration1
Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114
Langerhans cells (LC) belong to the dendritic cell family and
mediate Ag presentation in the cornea and ocular surface. Under normal
physiological conditions, the central cornea is devoid of LC.
Centripetal migration of LC plays a critical role in promoting
immunoinflammatory responses in the eye including allograft rejection
and herpetic keratitis. The molecular mechanisms responsible for ocular
LC migration are poorly understood. To examine whether TNF-
mediates
corneal LC migration and to establish the interaction of IL-1 and
TNF- in regulating LC migratory capacity, we utilized gene-targeted
knockout mice lacking IL-1 receptor I (IL-1RI-/-), TNF
receptor I (p55-/-), TNF receptor II
(p75-/-), or both
(p55-/-p75-/-). LC migration was induced by
thermal cautery or cytokine injection and enumerated by an
immunofluorescence assay. Migration of LC after cauterization and
TNF- injection was significantly depressed in both
p55-/- and p75-/- mice. Similarly, in the
first 72 h after intracorneal injection of IL-1, LC migration
was reduced in p55-/-, p75-/-, and
p55-/-p75-/- mice. In contrast, injection
of TNF- in IL-1RI-/- mice led to normal migration of
corneal LC indistinguishable from wild-type controls. These results
suggest that the IL-1 induction of corneal LC migration is largely
mediated by TNFR function, whereas TNF- induction of LC migration is
independent of IL-1RI activity. Moreover, the data suggest that both
p55 and p75 signaling pathways are important in mediating LC migration
in the cornea.
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