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      Galectin-1, an alternative signal for T cell death, is increased in activated macrophages

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          Abstract

          Galectin-1 belongs to an evolutionarily conserved family of animal ß-galactoside-binding proteins, which exert their functions by crosslinking the oligosaccharides of specific glycoconjugate ligands. During the past decade, attempts to identify the functional role of galectin-1 suggested participation in the regulation of the immune response. Only in the last few years has the molecular mechanism involved in these properties been clearly elucidated, revealing a critical role for galectin-1 as an alternative signal in the generation of T cell death. In the present study we will discuss the latest advances in galectin research in the context of the regulation of the immune response, not only at the central level but also at the periphery. Moreover, we will review the purification, biochemical properties and functional significance of a novel galectin-1-like protein from activated rat macrophages, whose expression is differentially regulated according to the activation state of the cells. The novel role of a carbohydrate-binding protein in the regulation of apoptosis is providing a breakthrough in galectin research and extending the interface between immunology, glycobiology and clinical medicine.

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          Most cited references71

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          Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis.

          Fas antigen is a cell-surface protein that mediates apoptosis. It is expressed in various tissues including the thymus and has structural homology with a number of cell-surface receptors, including tumour necrosis factor receptor and nerve growth factor receptor. Mice carrying the lymphoproliferation (lpr) mutation have defects in the Fas antigen gene. The lpr mice develop lymphadenopathy and suffer from a systemic lupus erythematosus-like autoimmune disease, indicating an important role for Fas antigen in the negative selection of autoreactive T cells in the thymus.
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            Mechanisms and genes of cellular suicide.

            H Steller (1995)
            Apoptosis is a morphologically distinct form of programmed cell death that plays a major role during development, homeostasis, and in many diseases including cancer, acquired immunodeficiency syndrome, and neurodegenerative disorders. Apoptosis occurs through the activation of a cell-intrinsic suicide program. The basic machinery to carry out apoptosis appears to be present in essentially all mammalian cells at all times, but the activation of the suicide program is regulated by many different signals that originate from both the intracellular and the extracellular milieu. Genetic studies in the nematode Caenorhabditis elegans and in the fruit fly Drosophila melanogaster have led to the isolation of genes that are specifically required for the induction of programmed cell death. At least some components of the apoptotic program have been conserved among worms, insects, and vertebrates.
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              The proto-oncogene Bcl-2 and its role in regulating apoptosis.

              G Kroemer (1997)
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                Author and article information

                Journal
                bjmbr
                Brazilian Journal of Medical and Biological Research
                Braz J Med Biol Res
                Associação Brasileira de Divulgação Científica (Ribeirão Preto, SP, Brazil )
                0100-879X
                1414-431X
                May 1999
                : 32
                : 5
                : 557-567
                Affiliations
                [01] orgnameUniversidad Nacional de Córdoba orgdiv1 Laboratorio de Inmunología, Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas
                Article
                S0100-879X1999000500009 S0100-879X(99)03200509
                10.1590/S0100-879X1999000500009
                972538f6-c60b-4993-adf8-d59455d2e346

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 17 November 1998
                : 10 February 1999
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 67, Pages: 11
                Product

                SciELO Brazil


                macrophage,galectin-1,apoptosis,immunomodulation
                macrophage, galectin-1, apoptosis, immunomodulation

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