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Differential roles of galectin-1 and galectin-3 in regulating leukocyte viability and cytokine secretion

Stowell, Sean R.; Qian, Yuning LU ; Karmakar, Sougata; Koyama, Natalia S.; Dias-Baruffi, Marcelo; Leffler, Hakon LU ; McEver, Rodger P. and Cummings, Richard D. (2008) In Journal of Immunology 180(5). p.3091-3102
Abstract
Galectin-1 (Gal-1) and galectin-3 (Gal-3) exhibit profound but unique immunomodulatory activities in animals but their molecular mechanisms are incompletely understood. Early studies suggested that Gal-1 inhibits leukocyte function by inducing apoptotic cell death and removal, but recent studies show that some galectins induce exposure of the common death signal phosphatidylserine (PS) independently of apoptosis. In tfhis study, we report that Gal-3, but not Gal-1, induces both PS exposure and apoptosis in primary activated human T cells, whereas both Gal-1 and Gal-3 induce PS exposure in neutrophils in the absence of cell death. Gal-1 and Gal-3 bind differently to the surfaces of T cells and only Gal-3 mobilizes intracellular Ca2+ in... (More)
Galectin-1 (Gal-1) and galectin-3 (Gal-3) exhibit profound but unique immunomodulatory activities in animals but their molecular mechanisms are incompletely understood. Early studies suggested that Gal-1 inhibits leukocyte function by inducing apoptotic cell death and removal, but recent studies show that some galectins induce exposure of the common death signal phosphatidylserine (PS) independently of apoptosis. In tfhis study, we report that Gal-3, but not Gal-1, induces both PS exposure and apoptosis in primary activated human T cells, whereas both Gal-1 and Gal-3 induce PS exposure in neutrophils in the absence of cell death. Gal-1 and Gal-3 bind differently to the surfaces of T cells and only Gal-3 mobilizes intracellular Ca2+ in these cells, although Gal-1 and Gal-3 bind their respective T cell ligands with similar affinities. Although Gal-1 does not alter T cell viability, it induces IL-10 production and attenuates IFN-gamma production in activated T cells, suggesting a mechanism for Gal-1-mediated immunosuppression in vivo. These studies demonstrate that Gal-1 and Gal-3 induce differential responses in T cells and neutrophils, and identify the first factor, Gal-3, capable of inducing PS exposure with or without accompanying apoptosis in different leukocytes, thus providing a possible mechanism for galectin-mediated immunomodulation in vivo. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Immunology
volume
180
issue
5
pages
3091 - 3102
publisher
American Association of Immunologists
external identifiers
  • wos:000256730000047
  • scopus:46949103440
ISSN
1550-6606
language
English
LU publication?
yes
id
25ac4aaa-f466-4c42-bf6d-5a83a2006d4a (old id 1191337)
alternative location
http://www.jimmunol.org/cgi/content/full/180/5/3091
date added to LUP
2008-09-08 14:21:49
date last changed
2017-09-17 06:45:14
@article{25ac4aaa-f466-4c42-bf6d-5a83a2006d4a,
  abstract     = {Galectin-1 (Gal-1) and galectin-3 (Gal-3) exhibit profound but unique immunomodulatory activities in animals but their molecular mechanisms are incompletely understood. Early studies suggested that Gal-1 inhibits leukocyte function by inducing apoptotic cell death and removal, but recent studies show that some galectins induce exposure of the common death signal phosphatidylserine (PS) independently of apoptosis. In tfhis study, we report that Gal-3, but not Gal-1, induces both PS exposure and apoptosis in primary activated human T cells, whereas both Gal-1 and Gal-3 induce PS exposure in neutrophils in the absence of cell death. Gal-1 and Gal-3 bind differently to the surfaces of T cells and only Gal-3 mobilizes intracellular Ca2+ in these cells, although Gal-1 and Gal-3 bind their respective T cell ligands with similar affinities. Although Gal-1 does not alter T cell viability, it induces IL-10 production and attenuates IFN-gamma production in activated T cells, suggesting a mechanism for Gal-1-mediated immunosuppression in vivo. These studies demonstrate that Gal-1 and Gal-3 induce differential responses in T cells and neutrophils, and identify the first factor, Gal-3, capable of inducing PS exposure with or without accompanying apoptosis in different leukocytes, thus providing a possible mechanism for galectin-mediated immunomodulation in vivo.},
  author       = {Stowell, Sean R. and Qian, Yuning and Karmakar, Sougata and Koyama, Natalia S. and Dias-Baruffi, Marcelo and Leffler, Hakon and McEver, Rodger P. and Cummings, Richard D.},
  issn         = {1550-6606},
  language     = {eng},
  number       = {5},
  pages        = {3091--3102},
  publisher    = {American Association of Immunologists},
  series       = {Journal of Immunology},
  title        = {Differential roles of galectin-1 and galectin-3 in regulating leukocyte viability and cytokine secretion},
  volume       = {180},
  year         = {2008},
}