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Prepublished online as a Blood First Edition Paper on October 24, 2002; DOI 10.1182/blood-2002-05-1339.
Submitted May 7, 2002
Accepted October 14, 2002
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*
Department of Oncological Sciences, University of Turin, Turin, Italy; Laboratory of Cancer Immunology, Institute for Cancer Research and Treatment, Turin, Italy
Divisione Universitaria di Immunologia Clinica e Ematologia, Ospedale Mauriziano Umberto I, Turin, Italy; Laboratory of Cancer Immunology, Institute for Cancer Research and Treatment, Turin, Italy
Divisione Universitaria di Immunologia Clinica e Ematologia, Ospedale Mauriziano Umberto I, Turin, Italy; Department of Oncological Sciences, University of Turin, Turin, Italy; Laboratory of Cancer Immunology, Institute for Cancer Research and Treatment, Turin, Italy
* Corresponding author; email: fcaligaris{at}mauriziano.it.
Growth and survival of chronic B-cell tumors are favoured by the malignant cell capacity to respond to selected microenvironmental stimuli provided by non-tumoral bystander cells. To investigate which mechanisms operate in these crosstalks and whether they are malignancy-related or reproduce the mechanisms utilized 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 here demonstrate that: i) leukemic and normal CD5+ B lymphocytes uniformly express CD100; ii) 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; iii) 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 utilized by normal CD5+ B cells.
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