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Blood, Vol. 94 No. 12 (December 15), 1999:
pp. 4195-4201
Differential In Situ Cytokine Profiles of Langerhans-Like Cells and T
Cells in Langerhans Cell Histiocytosis: Abundant Expression of
Cytokines Relevant to Disease and Treatment
R. Maarten Egeler,
Blaise E. Favara,
Marjan van Meurs,
Jon D. Laman, and
Eric Claassen
From the Southern Alberta Children's Cancer Program, Alberta
Children's Hospital/Tom Baker Cancer Centre, Department of Oncology
and Pediatrics, University of Calgary, Calgary, Alberta, Canada; the
Department of Pediatric Oncology (Sophia Children's Hospital) and the
Department of Immunology, Erasmus University, Rotterdam, The
Netherlands; the Laboratory for Persistent Viral Diseases, Rocky
Mountain Laboratories, National Institutes of Health, Hamilton, MT; the
Department of Pathology, University of Utah, Salt Lake City, UT; and
the ID-DLO Institute for Animal Science and Health, Department of
Immunology, Lelystad, The Netherlands.
The pathogenesis of Langerhans cell histiocytosis (LCH) remains
poorly understood. To further elucidate LCH pathogenesis, we analyzed
the expression of 10 cytokines relevant to cellular recruitment and
activation at the protein level in 14 patients and identified the
lesional cells responsible for cytokine production in situ by
immunohistochemistry. The cytokines investigated included the
hematopoietic growth factors interleukin-3 (IL-3), IL-7, and granulocyte-macrophage colony-stimulating factor (GM-CSF); the lymphocyte regulatory cytokines IL-2, IL-4, and IL-10; the inflammatory regulators IL-1 and tumor necrosis factor- (TNF-); and the effector cell-activating cytokines IL-5 and interferon-
(IFN-). In all specimens, CD1a+ histiocytes
(LCH cells) and CD3+ T cells produced large amounts of
cytokines, creating a true cytokine storm. IL-2, IL-4, IL-5, and
TNF- were produced exclusively by T cells, whereas only IL-1 was
produced by LCH cells. Equal numbers of LCH cells, T cells, and
macrophages produced GM-CSF and IFN-. Equal numbers of LCH cells and
macrophages produced IL-10, whereas IL-3 was produced by T cells and
macrophages. IL-7 was only produced by macrophages. Eosinophils,
present in some specimens, were partially responsible for the
production of IL-5, IFN-, GM-CSF, IL-10, IL-3, and IL-7. Expression
of all cytokines, abundant in most biopsies, was irrespective of age,
gender, or site of biopsy. These findings emphasize the role of T cells
in LCH. The juxtaposition of T cells and LCH cells suggests that both
cells interact in a cytokine amplification cascade, resulting from
stimulation of autocrine and paracrine stimulatory loops. This cascade
can be linked directly to the development of LCH through recruitment,
maturation, and proliferation of LCH cells. The cytokines studied are
known to be involved in the development of other characteristic
features of LCH, such as fibrosis, necrosis, and osteolysis.
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