Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Mantle cell lymphomas acquire increased expression of CCL4, CCL5 and 4-1BB-L implicated in cell survival

Ek, Sara LU ; Bjorck, Erik ; Högerkorp, Carl-Magnus LU ; Nordenskjold, Magnus ; Porwit-Macdonald, Anna and Borrebaeck, Carl LU (2006) In International Journal of Cancer 118(8). p.2092-2097
Abstract
We have analyzed mantle cell lymphomas (MCLs), using high-density DNA microarrays, and confirmed the expression of differentially regulated antigens, using flow cytometry and immunohistochemistry. The results show that MCLs acquire expression of molecules that normally are involved in interaction with other immune cells and, thus, might affect the ability of the tumor to survive. The MCL signature is represented by the overexpression of the chemokine CCL4 (MIP-1), implicated in the recruitment of regulatory T cells, as well as CCL5 and 4-1BB-L. The latter molecules are normally involved in chemotaxis of T cells and B cell activation, respectively. Signaling through 4-1BB-L allows B cells to proliferate and the expression of its ligand, by... (More)
We have analyzed mantle cell lymphomas (MCLs), using high-density DNA microarrays, and confirmed the expression of differentially regulated antigens, using flow cytometry and immunohistochemistry. The results show that MCLs acquire expression of molecules that normally are involved in interaction with other immune cells and, thus, might affect the ability of the tumor to survive. The MCL signature is represented by the overexpression of the chemokine CCL4 (MIP-1), implicated in the recruitment of regulatory T cells, as well as CCL5 and 4-1BB-L. The latter molecules are normally involved in chemotaxis of T cells and B cell activation, respectively. Signaling through 4-1BB-L allows B cells to proliferate and the expression of its ligand, by the intra-tumoral mesh of follicular dendritic cells (FDC), could thus serve as a paracrine loop facilitating growth and survival of MCL cells. (Less)
Please use this url to cite or link to this publication:
author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
International Journal of Cancer
volume
118
issue
8
pages
2092 - 2097
publisher
John Wiley & Sons Inc.
external identifiers
  • wos:000236397200035
  • pmid:16287062
  • scopus:33645241144
ISSN
0020-7136
DOI
10.1002/ijc.21579
language
English
LU publication?
yes
id
260b6a61-a414-4b67-a640-ed04616e9dc3 (old id 147959)
date added to LUP
2016-04-01 12:23:07
date last changed
2022-04-13 18:17:17
@article{260b6a61-a414-4b67-a640-ed04616e9dc3,
  abstract     = {{We have analyzed mantle cell lymphomas (MCLs), using high-density DNA microarrays, and confirmed the expression of differentially regulated antigens, using flow cytometry and immunohistochemistry. The results show that MCLs acquire expression of molecules that normally are involved in interaction with other immune cells and, thus, might affect the ability of the tumor to survive. The MCL signature is represented by the overexpression of the chemokine CCL4 (MIP-1), implicated in the recruitment of regulatory T cells, as well as CCL5 and 4-1BB-L. The latter molecules are normally involved in chemotaxis of T cells and B cell activation, respectively. Signaling through 4-1BB-L allows B cells to proliferate and the expression of its ligand, by the intra-tumoral mesh of follicular dendritic cells (FDC), could thus serve as a paracrine loop facilitating growth and survival of MCL cells.}},
  author       = {{Ek, Sara and Bjorck, Erik and Högerkorp, Carl-Magnus and Nordenskjold, Magnus and Porwit-Macdonald, Anna and Borrebaeck, Carl}},
  issn         = {{0020-7136}},
  language     = {{eng}},
  number       = {{8}},
  pages        = {{2092--2097}},
  publisher    = {{John Wiley & Sons Inc.}},
  series       = {{International Journal of Cancer}},
  title        = {{Mantle cell lymphomas acquire increased expression of CCL4, CCL5 and 4-1BB-L implicated in cell survival}},
  url          = {{http://dx.doi.org/10.1002/ijc.21579}},
  doi          = {{10.1002/ijc.21579}},
  volume       = {{118}},
  year         = {{2006}},
}