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Blood, 1 March 2001, Vol. 97, No. 5, pp. 1241-1248
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Differentiation of Langerhans cells in Langerhans cell
histiocytosis
Frederic Geissmann,
Yves Lepelletier,
Sylvie Fraitag,
Jenny Valladeau,
Christine Bodemer,
Marianne Debré,
Michelle Leborgne,
Sem Saeland, and
Nicole Brousse
From the Institut Fédératif de Recherche
Necker-Enfants Malades (Service d'Anatomie Pathologique EA 219, Unité Mixte de Recherche 8603 CNRS/Université Paris-V,
Service de Dermatologie, Unité d'Immunologie et
d'Hématologie Pédiatrique), Hôpital Necker-Enfants
Malades, Faculté Necker, Université Paris-V René
Descartes, Paris, France; and Schering-Plough Laboratory for
Immunological Research, Dardilly, France.
Langerhans cell histiocytosis (LCH) consists of lesions composed of
cells with a dendritic Langerhans cell (LC) phenotype. The clinical
course of LCH ranges from spontaneous resolution to a chronic and
sometimes lethal disease. We studied 25 patients with various clinical
forms of the disease. In bone and chronic lesions, LCH cells had
immature phenotype and function. They coexpressed LC antigens CD1a and
Langerin together with monocyte antigens CD68 and CD14. Class II
antigens were intracellular and LCH cells almost never expressed CD83
or CD86 or dendritic cell (DC)-Lamp, despite their CD40 expression.
Consistently, LCH cells sorted from bone lesions (eosinophilic
granuloma) poorly stimulated allogeneic T-cell proliferation in vitro.
Strikingly, however, in vitro treatment with CD40L induced the
expression of membrane class II and CD86 and strongly increased LCH
cell allostimulatory activity to a level similar to that of mature DCs.
Numerous interleukin-10-positive (IL-10+),
Langerin , and CD68+ macrophages were
found within bone and lymph node lesions. In patients with self-healing
and/or isolated cutaneous disease, LCH cells had a more mature
phenotype. LCH cells were frequently CD14 and
CD86+, and macrophages were rare or absent, as were
IL-10-expressing cells. We conclude that LCH cells in the bone and/or
chronic forms of the disease accumulate within the tissues in an
immature state and that most probably result from extrinsic signals and
may be induced to differentiate toward mature DCs after CD40
triggering. Drugs that enhance the in vivo maturation of these immature
DCs, or that induce their death, may be of therapeutic benefit.
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