Beta-galactoside-binding protein secreted by activated T cells inhibits antigen-induced proliferation of T cells.

Blaser, Claudine; Kaufmann, Martina; Mueller, Christoph; Zimmermann, Christine; Wells, Valerie; Mallucci, Livio; Pircher, Hanspeter (1998). Beta-galactoside-binding protein secreted by activated T cells inhibits antigen-induced proliferation of T cells. European journal of immunology, 28(8), pp. 2311-2319. Wiley-VCH 10.1002/(SICI)1521-4141(199808)28:08<2311::AID-IMMU2311>3.0.CO;2-G

[img] Text
Eur_J_Immunol_-_2006_-_Blaser_-__Galactoside_binding_protein_secreted_by_activated_T_cells_inhibits_antigen_induced.pdf - Published Version
Restricted to registered users only
Available under License Publisher holds Copyright.

Download (149kB) | Request a copy

We have used mRNA differential display PCR to search for genes induced in activated T cells and have found the LGALS1 (lectin, galactoside-binding, soluble) gene to be strongly up-regulated in effector T cells. The protein coded by the LGALS1 gene is a beta-galactoside-binding protein (betaGBP), which is released by cells as a monomeric negative growth factor but which can also associate into homodimers (galectin-1) with lectin properties. Northern blot analysis revealed that ex vivo isolated CD8+ effector T cells induced by a viral infection expressed high amounts of LGALS1 mRNA, whereas LGALS1 expression was almost absent in resting CD8+ T cells. LGALS1 expression could be induced in CD4+ and CD8+ T cells upon activation with the cognate peptide antigen and high levels of LGALS1 expression were found in concanavalin A-activated T cells but not in lipopolysaccharide-activated B cells. Gel filtration and Western blot analysis revealed that only monomeric betaGBP was released by activated CD8+ T cells and in vitro experiments further showed that recombinant betaGBP was able to inhibit antigen-induced proliferation of naive and antigen-experienced CD8+ T cells. Thus, these data indicate a role of betaGBP as an autocrine negative growth factor for CD8+ T cells.

Item Type:

Journal Article (Original Article)


04 Faculty of Medicine > Service Sector > Institute of Pathology

UniBE Contributor:

Müller, Christoph (C)


500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health








Christoph Müller

Date Deposited:

20 Sep 2022 13:49

Last Modified:

29 Mar 2023 23:38

Publisher DOI:


PubMed ID:





Actions (login required)

Edit item Edit item
Provide Feedback