Localization of Endogenous &amp;beta;-Galactoside-Binding Lectin in Human Cells and Tissues

Allen, Herbert B.; Sucato, Dan; Gottstine, Sally; Kisailus, Edward C.; Nava, Hector; Petrelli, Nicholas J.; Castillo, Nieva; Wilson, David I.

doi:10.1159/000217688

Cited by 32 publications

(24 citation statements)

References 16 publications

(31 reference statements)

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“…1) is consistent with prior reports (34,35) and indicates that many cell types may secrete galectin-1 in skin. We also observed galectin-1 immunoreactivity within the cytoplasm of CD7 Ϫ Sezary cells in skin lesions (Fig.…”

Section: Discussionsupporting

confidence: 92%

“…1B) suggested that the tumor cells synthesized galectin-1, as well as being exposed to abundant galectin-1 in the extracellular milieu. In the dermis, there were also scattered galectin-1 ϩ non-neoplastic cells, including fibroblasts, endothelial cells, and macrophages, as previously described (34,35).…”

Section: Galectin-1 Immunoreactivity In Mycosis Fungoides Biopsiessupporting

confidence: 67%

“…Absent PNA reactivity of Sezary cells contrasts with strong PNA reactivity of keratinocytes. [31][32][33][34][35], implying that Sezary cells may acquire resistance to endogenous pro-apoptotic galectins.…”

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confidence: 99%

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Galectin-1–Mediated Apoptosis in Mycosis Fungoides: The Roles of CD7 and Cell Surface Glycosylation

et al. 2003

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Sezary cells, the malignant T cells in mycosis fungoides/Sezary syndrome, resist a variety of apoptosis-inducing agents, a feature that contributes to the poor response to therapy in mycosis fungoides. Galectin-1 is a mammalian lectin that triggers T cell apoptosis. For T cells to be susceptible to galectin-1-induced apoptosis, the T cells must express specific glycoprotein receptors, such as CD7, that bear the specific oligosaccharides recognized by galectin-1. Because Sezary cells are characteristically CD7 ؊ , lack of CD7 expression has been proposed to render Sezary cells resistant to galectin-1-induced death. However, the role played by aberrant cell surface glycosylation in resistance of Sezary cells to galectin-1 has not been examined. In this study, we demonstrated abundant galectin-1 in mycosis fungoides skin lesions, indicating that Sezary cells are exposed to galectin-1 in vivo. To determine specific characteristics of Sezary cells that contribute to galectin-1 resistance, we assessed CD7 expression and cell surface glycosylation of Sezary cells in mycosis fungoides lesions and of four Sezary T cell lines. Sezary cells in primary lesions and Sezary T cell lines demonstrated a characteristic "glycotype" with sialylated core 1 O-glycans that promote galectin-1 resistance. Expression of CD7 was necessary but not sufficient for galectin-1-induced death of Sezary cell lines. In addition, CD7 ؊ Sezary cell lines, and Sezary cells within mycosis fungoides lesions, expressed galectin-1, whereas CD7-positive Sezary cell lines did not express galectin-1. We propose that both loss of CD7 expression and altered cellular glycosylation contribute to apoptosis resistance of malignant T cells in mycosis fungoides.

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Section: Discussionsupporting

confidence: 92%

Section: Galectin-1 Immunoreactivity In Mycosis Fungoides Biopsiessupporting

confidence: 67%

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Galectin-1–Mediated Apoptosis in Mycosis Fungoides: The Roles of CD7 and Cell Surface Glycosylation

et al. 2003

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“…4 Its presence has been localized within the central and peripheral immune compartment in thymic epithelial cells, 5 activated T cells 6,7 and activated macrophages. 8,9 It has also been found in immune privileged sites of the body such as placenta, 10,11 cornea 12 and testis. 13 Recent observations suggest that Gal-1 could play an important role in generating and maintaining central and peripheral immune tolerance.…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms implicated in galectin-1-induced apoptosis: activation of the AP-1 transcription factor and downregulation of Bcl-2

et al. 2000

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Galectins are emerging as a new class of bioactive molecules with specific immunomodulatory properties. Galectin-1 (Gal-1), a member of this family, has been shown to induce apoptosis of mature T cells and immature thymocytes. To gain insight into the intracellular signals transduced by Gal-1 upon binding to mature T cells, we investigated whether this protein triggered activation of the dimeric AP-1 transcription factor. A marked increase in the binding of nuclear extracts to synthetic oligonucleotides containing the AP-1 consensus sequence, could be detected by an electrophoretic mobility shift assay, when T cells were cultured for 30 min in the presence of Gal-1. This DNA-binding activity was preceded by a rapid increase in the levels of c-Jun mRNA, as determined by Northern blot analysis. Requirement of AP-1 for Gal-1-induced apoptosis was confirmed by the dosedependent reduction on the level of DNA fragmentation observed when cells were pre-treated with curcumin (an inhibitor of AP-1 activation) before exposure to Gal-1. Finally, evidence is also provided by Western blot analysis, showing that Gal-1 inhibits Concanavalin A (Con A) induction of Bcl-2 protein. Results presented in this study provide the first experimental evidence regarding AP-1 and Bcl-2 as targets of the signal transduction pathway triggered by Gal-1 and set the basis for a more in depth understanding of the molecular mechanisms of T-cell death regulation. Cell Death and Differentiation (2000) 7, 747 ± 753.

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“…Galectin-1 is also present in sites of immune privilege, such as placenta (Hirabayashi and Kasai, 1988;Iglesias et al, 1998a), cornea (Ogden et al, 1998) and prostate (Allen et al, 1991;Hirabayashi and Kasai, 1993). The presence of this protein in these vulnerable sites might contribute to mantain a state of tolerance by inducing apoptosis of inflammatory and activated T cells that could provoke injury, autoimmune damage or infection.…”

Section: Galectin-1 Expression In Immune Privileged Sites" a Novel Mementioning

confidence: 99%

“Galectin‐1 Induces Central and Peripheral Cell Death:Implications in T‐Cell Physiopathology”

Sotomayor

Rabinovich

2000

Journal of Immunology Research

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The immune system has a remarkable capacity to maintain a state of equilibrium even as it responds to a diverse array of foreign proteins and despite its contact exposure to self-antigens. Apoptosis is one of the mechanisms aimed at preserving the homeostasis after the completion of an immune response, thus returning the immune system to a basal state and warranting the elimination of autoagressive cells in both central and peripheral lymphoid organs. Targeted deletions in critical genes involved in the apoptotic death machinery together with natural spontaneous mutations have clearly shown the importance of apoptosis in the regulation of the immune response. This complex scenario of stimulatory and inhibitory genes has been enriched with the finding that galectin-1, a 14.5 kDa [3-galactoside-binding protein, is able to induce apoptosis of immature cortical thymocytes and mature T cells by cross-linking cell surface glycoconjugates. Galectin-1 is present not only in central and peripheral lymphoid organs, but also at sites of immune privilege. In the present article we will discuss the implications of galectin-1-induced apoptosis in T-cell physiopathology in an attempt to validate its therapeutic potential in autoimmune and inflammatory diseases.Keywords: galectin-1, apoptosis, immunomodulation, macrophages, autoimmunity INTRODUCTION Death, along with growth and differentiation, is a critical part of the life cycle of the cell. Homeostasis control of cell number is thought to be the result of the dynamic balance between cell proliferation and cell death. It is only in the past ten years, that the attention has been focused on the physiological occurrence of cell death and its role in the homeostasis.Apoptosis or programmed cell death, is a phenomenon that plays a crucial role in a myriad of physiological and pathological processes. This review will briefly cover some relevant aspects of programmed cell death in the immune system in an attempt to provide valuable information about new molecules responsible for triggering death signals, such as galectin-1. The implications of this protein will be discussed in the context of T cell physiology and the regulation of central and peripheral tolerance. Finally, novel and intriguing findings will also be discussed implicating the use of this carbohydrate-binding protein in the treatment of autoimmune and inflammatory diseases.

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Localization of Endogenous β-Galactoside-Binding Lectin in Human Cells and Tissues

Cited by 32 publications

References 16 publications

Galectin-1–Mediated Apoptosis in Mycosis Fungoides: The Roles of CD7 and Cell Surface Glycosylation

Galectin-1–Mediated Apoptosis in Mycosis Fungoides: The Roles of CD7 and Cell Surface Glycosylation

Molecular mechanisms implicated in galectin-1-induced apoptosis: activation of the AP-1 transcription factor and downregulation of Bcl-2

“Galectin‐1 Induces Central and Peripheral Cell Death:Implications in T‐Cell Physiopathology”

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