Differential roles of galectin-1 and galectin-3 in regulating leukocyte viability and cytokine secretion
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1191337
- author
- Stowell, Sean R. ; Qian, Yuning LU ; Karmakar, Sougata ; Koyama, Natalia S. ; Dias-Baruffi, Marcelo ; Leffler, Hakon LU ; McEver, Rodger P. and Cummings, Richard D.
- organization
- publishing date
- 2008
- 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
- 2016-04-01 14:20:47
- date last changed
- 2022-04-14 17:16:52
@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}},
url = {{http://www.jimmunol.org/cgi/content/full/180/5/3091}},
volume = {{180}},
year = {{2008}},
}