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*
Institut National de la Santé et de la Recherche Médicale U82, Unité de Formation et de Recherche Xavier Bichat, Paris, France;
Service de Pneumologie, Hôpital Avicenne, Bobigny, France; and
Service de Pneumologie, Hôpital Charles Nicolle, Rouen, France
Because Langerhans cells (LC) in peripheral tissues are generally
"immature" cells with poor lymphostimulatory activity, the
contribution of immune responses initiated by LC to the pathogenesis of
pulmonary LC histiocytosis (LCH) has been uncertain. In this study we
demonstrate that LC accumulating in LCH granulomas are phenotypically
similar to mature lymphostimulatory dendritic cells present in lymphoid
organs. LC in LCH granulomas intensely expressed B7-1 and B7-2
molecules, whereas normal pulmonary LC and LC accumulating in other
pathologic lung disorders did not express these costimulatory
molecules. The presence of B7+ LC in LCH granulomas was
associated with the expression in these lesions, but not at other sites
in the lung, of a unique profile of cytokines (presence of GM-CSF,
TNF-
, and IL-1ß and the absence of IL-10) that is known to promote
the in vitro differentiation of LC into cells expressing a
lymphostimulatory phenotype. Finally, LCH granulomas were the only site
where CD154-positive T cells could be identified in close contact with
LC intensely expressing CD40 Ags. Taken together, these results
strongly support the idea that an abnormal immune response initiated by
LC may participate in the pathogenesis of pulmonary LCH, and suggest
that therapeutic strategies aimed at modifying the lymphostimulatory
phenotype of LC may be useful in the treatment of this
disorder.
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