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Prepublished online as a Blood First Edition Paper on October 24, 2002; DOI 10.1182/blood-2002-05-1339.
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Blood, 1 March 2003, Vol. 101, No. 5, pp. 1962-1969
NEOPLASIA
CD100/Plexin-B1 interactions sustain proliferation and survival
of normal and leukemic CD5+ B lymphocytes
Luisa Granziero,
Paola Circosta,
Cristina Scielzo,
Elisa Frisaldi,
Stefania Stella,
Massimo Geuna,
Silvia Giordano,
Paolo Ghia, and
Federico Caligaris-Cappio
From the Department of Oncological Sciences,
University of Torino, Institute for Cancer Research and
Treatment (IRCC), Candiolo (TO) and Division of Clinical Immunology and
Hematology, Ospedale Mauriziano Umberto I, Torino, Italy.
Growth and survival of chronic B-cell tumors are favored by the
malignant cell's capacity to respond to selected microenvironmental stimuli provided by nontumoral bystander cells. To investigate which
mechanisms operate in these crosstalks and whether they are
malignancy-related or reproduce the mechanisms used by normal B cells
we have studied the expression and functional role of semaphorin CD100
(now called Sema4D) in chronic lymphocytic leukemia (CLL) cells and
normal CD5+ B cells. We demonstrate here that (1) leukemic
and normal CD5+ B lymphocytes uniformly express CD100; (2)
the CD100 high-affinity receptor Plexin-B1 is expressed by bone marrow
stromal cells, follicular dendritic cells, and activated T lymphocytes,
and is thus available to CD100+ lymphocytes in different
specific microenvironments; and (3) upon interaction between CD100 and
Plexin-B1 both CLL and normal CD5+ B cells increase their
proliferative activity and extend their life span. These findings
establish that Plexin-B1 is an easily accessible receptor for CD100
within the immune system. The encounter of CD100+ leukemic
cells with Plexin-B1 may promote the proliferation and survival of
malignant cells. The crosstalk operated by the CD100/Plexin-B1 interaction is not malignancy related but reproduces a mechanism used
by normal CD5+ B cells.
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