Amelioration of graft versus host disease by galectin-1

Baum, Linda G.; Blackall, Douglas P.; Arias-Magallano, Sarah; Nanigian, Danielle; Uh, Soo Y; Browne, Jordan M; Hoffmann, Douglas; Emmanouilides, Christos; Territo, Mary; Baldwin, Gayle Cocita

doi:10.1016/j.clim.2003.08.003

Cited by 119 publications

(134 citation statements)

References 44 publications

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“…Our observations regarding Gal1 function in cHL are consistent with reports regarding the role of the lectin in murine models of Th1-driven chronic inflammatory and autoimmune disorders, including collagen-induced arthritis, inflammatory bowel disease, graft vs. host disease, and autoimmune uveitis (17)(18)(19)(20). In these studies, the administration of Gal1 dramatically suppressed Th1-dependent responses and skewed toward Th2 cytokine profiles (17)(18)(19)(20)29).…”

Section: Discussionsupporting

confidence: 80%

“…In these studies, the administration of Gal1 dramatically suppressed Th1-dependent responses and skewed toward Th2 cytokine profiles (17)(18)(19)(20)29). A careful examination of the mechanisms involved in Gal1-mediated Th2 skewing recently revealed that Th1 cells express the repertoire of cell surface glycans required for Gal1 binding and subsequent cell death, whereas Th2 cells are protected from Gal1 by differential sialylation of their cell surface glycoproteins (30).…”

Section: Discussionmentioning

confidence: 99%

“…Through binding and cross-linking of specific glycoconjugates, Gal1 has the potential to inhibit T cell effector functions and regulate the inflammatory response (16)(17)(18)(19)(20). In several murine models of chronic inflammatory diseases, recombinant Gal1 suppressed Th1-dependent responses and increased T cell susceptibility to activation-induced cell death (17)(18)(19)(20).…”

mentioning

confidence: 99%

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The AP1-dependent secretion of galectin-1 by Reed–Sternberg cells fosters immune privilege in classical Hodgkin lymphoma

Juszczyński

Ouyang

Monti

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

290

301

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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The AP1-dependent secretion of galectin-1 by Reed–Sternberg cells fosters immune privilege in classical Hodgkin lymphoma

Juszczyński

Ouyang

Monti

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

290

301

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“…Its up-regulation in tumors correlates with poor clinical outcome, possibly because galectin-1 reduces the survival of tumor resident T cells and promotes tumor immune escape (19). In addition, galectin-1 has been implicated in transplantation tolerance because it diminishes morbidity and mortality of graft-versus-host disease in a mouse allogeneic bone marrow transplantation model (20).Galectin-1 is up-regulated in uterine natural killer cells and is a key moderator of regulatory T cell functions (21,22). A recent study reported that galectin-1 induces the generation of tolerogenic dendritic cells and regulatory T cells in mice, and the knockout of LGALS1 led to a higher rate of fetal loss in allogeneic mating (9).…”

mentioning

confidence: 99%

Emergence of hormonal and redox regulation of galectin-1 in placental mammals: Implication in maternal–fetal immune tolerance

Than

Romero²,

Erez³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Galectin-1 is an anti-inflammatory lectin with pleiotropic regulatory functions at the crossroads of innate and adaptive immunity. It is expressed in immune privileged sites and is implicated in establishing maternal-fetal immune tolerance, which is essential for successful pregnancy in eutherian mammals. Here, we show conserved placental localization of galectin-1 in primates and its predominant expression in maternal decidua. Phylogenetic footprinting and shadowing unveil conserved cis motifs, including an estrogen responsive element in the 5 promoter of LGALS1, that were gained during the emergence of placental mammals and could account for sex steroid regulation of LGALS1 expression, thus providing additional evidence for the role of galectin-1 in immuneendocrine cross-talk. Maximum parsimony and maximum likelihood analyses of 27 publicly available vertebrate and seven newly sequenced primate LGALS1 coding sequences reveal that intense purifying selection has been acting on residues in the carbohydrate recognition domain and dimerization interface that are involved in immune functions. Parsimony-and codon model-based phylogenetic analysis of coding sequences show that amino acid replacements occurred in early mammalian evolution on key residues, including gain of cysteines, which regulate immune functions by redox status-mediated conformational changes that disable sugar binding and dimerization, and that the acquired immunoregulatory functions of galectin-1 then became highly conserved in eutherian lineages, suggesting the emergence of hormonal and redox regulation of galectin-1 in placental mammals may be implicated in maternal-fetal immune tolerance.decidua ͉ estrogen ͉ glycocode ͉ immune-endocrine cross-talk ͉ pregnancy T he success of mammalian pregnancy, in which the developing fetus and mother exchange nutrients, gases, and other molecules via the chorioallantoic placenta, requires maternal immune tolerance to fetal allo-antigens (1-4). This tolerance presumably prevents the occurrence of exaggerated inflammation at the implantation site and reduces the danger of destructive immune attacks on the fetus, a danger that the first mammals with an invasive placenta would have faced (5, 6). It seems likely that mechanisms for immune tolerance to invasive placentation were already functioning in the early placental mammals and that immunoregulatory molecules, which had existed before the mammalian placenta evolved, were incorporated in this tolerance and have undergone evolutionary modifications coincident with the emergence of the mammalian placenta. Here, we present evidence that such modifications occurred in a key immunoregulatory molecule, galectin-1.Molecules that have been implicated in conferring maternalfetal immune tolerance include galectin-1, B7 proteins, Crry, Fas ligand, HLA-G, indoleamine 2,3-dioxygenase, and killer cell immunoglobulin-like receptors (2-4, 7-11). These proteins are involved in pathways regulating adaptive or innate immune responses at the maternal-fetal interface, and their di...

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“…Clinical ocular pathology can also be prevented by the administration of recombinant Galectin-1 (rGal-1) either early or late during the course of EAU. Galectin-1 is a member of a highly conserved protein family (25) , expressed at sites of T-cell activation and immune privilege (26)(27) , and has the potential to regulate inflammatory responses (28)(29)(30)(31)(32)(33)(34) . The treatment with rGal-1 in IRBP-induced EAU in B10.RIII mice resulted in significant amelioration of ocular inflammation.…”

Section: New Therapies In Eaumentioning

confidence: 99%

Autoimmune uveitis: study of treatment therapies

Commodaro

Moraes

Tambourgi

et al. 2010

Einstein (São Paulo)

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Experimental autoimmune uveitis is an organ-specific T-cell mediated autoimmune disease characterized by inflammation and consequent destruction of the neural retina and adjacent tissues. Inflammation in experimental autoimmune uveitis may be induced in rodents by immunization with retinal antigens, such as interphotoreceptor retinoid-binding protein. We present a review of experimental studies that correlate primary immunobiological functions with this chronic disease and the possible use of molecules for the treatment of autoimmune uveitis.

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Amelioration of graft versus host disease by galectin-1

Cited by 119 publications

References 44 publications

The AP1-dependent secretion of galectin-1 by Reed–Sternberg cells fosters immune privilege in classical Hodgkin lymphoma

The AP1-dependent secretion of galectin-1 by Reed–Sternberg cells fosters immune privilege in classical Hodgkin lymphoma

Emergence of hormonal and redox regulation of galectin-1 in placental mammals: Implication in maternal–fetal immune tolerance

Autoimmune uveitis: study of treatment therapies

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