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Blood, 1 September 2002, Vol. 100, No. 5, pp. 1715-1720
IMMUNOBIOLOGY
Peripheral blood but not tissue dendritic cells express CD52 and
are depleted by treatment with alemtuzumab
Andrea G. S. Buggins,
Ghulam J. Mufti,
Jonathan Salisbury,
Jane Codd,
Nigel Westwood,
Matthew Arno,
Keith Fishlock,
Antonio Pagliuca, and
Stephen Devereux
From the Departments of Haematological Medicine and
Histopathology, Guy's, King's and Thomas' School of Medicine,
Denmark Hill, London, England.
CAMPATH antibodies recognize CD52, a phosphatidylinositol-linked
membrane protein expressed by mature lymphocytes and monocytes. Since
some antigen-presenting dendritic cells (DCs) differentiate from a
monocytic progenitor, we investigated the expression of CD52 on
dendritic cell subsets. Four-color staining for lineage markers (CD3,
14, 16, 19, 20, 34, and 56), HLA-DR, CD52, and CD123 or CD11c
demonstrated that myeloid peripheral blood (PB) DCs, defined as
lineage HLA-DR+CD11c+,
express CD52, while expression by CD123+ lymphoid DCs was
variable. Depletion of CD52+ cells from normal PB strongly
inhibited their stimulatory activity in an allogeneic mixed lymphocyte
reaction and also reduced the primary autologous response to the potent
neoantigen keyhole limpet hemocyanin. CD52 is thus expressed by
a myeloid subset of PBDCs that is strongly allostimulatory and capable
of initiating a primary immune response to soluble antigen.
Administration of alemtuzumab, a humanized monoclonal antibody against
CD52, to patients with lymphoproliferative disorders or as
conditioning for hematopoietic stem cell transplantation resulted
in a marked reduction in circulating lineageHLA-DR+ DCs (mean 31-fold reduction,
P = .043). Analysis of monocyte-derived DCs in vitro
revealed a reduction in CD52 expression during culture in
granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4, with complete loss following activation-induced maturation with lipopolysaccharide. In contrast to the findings in PB,
epidermal and small-intestine DCs did not express CD52, suggesting
either that transit from blood to epidermis and gut is associated with
loss of CD52 or that DCs in these tissues originate from another
population of cells.
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