O-Glycosylation Regulates LNCaP Prostate Cancer Cell Susceptibility to Apoptosis Induced by Galectin-1

Valenzuela, Héctor; Pace, Karen E.; Cabrera, Paula; White, Rachel; Porvari, Katja; Kaija, Helena; Vihko, Pirkko; Baum, Linda G.

doi:10.1158/0008-5472.can-05-4431

Cited by 79 publications

(64 citation statements)

References 44 publications

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“…1-4) (26, 29, 30), we sought to determine whether iGal-1 might induce additional previously described biological endpoints in T cells. Similar to previous results with Gal-1 (24,26,46,61,62), iGal-1 induced apoptotic cell death in T leukemic CEM cells (Fig. 9, A and B) and MOLT-4 cells (data not shown) only in the presence of DTT in a dose-dependent manner (Fig.…”

Section: Igal-1 Retains Biological Activity Toward T Cellssupporting

confidence: 91%

Differential Roles of Galectin-1 and Galectin-3 in Regulating Leukocyte Viability and Cytokine Secretion

Stowell

Qian

Karmakar

et al. 2008

The Journal of Immunology

226

189

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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 this 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-γ 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.

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Section: Igal-1 Retains Biological Activity Toward T Cellssupporting

confidence: 91%

Differential Roles of Galectin-1 and Galectin-3 in Regulating Leukocyte Viability and Cytokine Secretion

Stowell

Qian

Karmakar

et al. 2008

The Journal of Immunology

226

189

View full text Add to dashboard Cite

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“…Preventing Bim-mediated cell death by either Bim deficiency or forced expression of Bcl-2, a protein shown to counteract the proapoptotic activity of Bim, renders the T eff cells resistant to T reg cellmediated suppression in vitro and in vivo. In this context, it is notable that the galectins also mediate cell death by a perforin-and granzyme-independent mechanism, which suggests a potential link between these two pathways 33,34 . Unfortunately, it is difficult to explain bystander suppression or infectious tolerance in vivo on the basis of these T eff cell-killing activities.…”

Section: T Reg Cells Influence Other T Cellsmentioning

confidence: 99%

The Foxp3+ regulatory T cell: a jack of all trades, master of regulation

2008

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The function of regulatory T cells (T reg cells) has been attributed to a growing number of diverse pathways, molecules and processes. Seemingly contradictory conclusions regarding the mechanisms underlying T reg cell suppressive activity have revitalized skeptics in the field who challenge the core validity of the idea of T reg cells as central immune regulators. However, we note that a consensus may be emerging from the data: that multiple T reg cell functions act either directly or indirectly at the site of antigen presentation to create a regulatory milieu that promotes bystander suppression and infectious tolerance. Thus, the versatility and adaptability of the Foxp3 + T reg cells may in fact be the best argument that these cells are 'multitalented masters of immune regulation'.Armed with the potential to destroy invading microorganisms and stop aberrant outgrowth of tumor cells, the immune system has extensive built-in mechanisms for preventing attack of healthy self tissues. The first line of such 'self-tolerance' is the elimination of selfreactive T lymphocytes and B lymphocytes during negative selection in the thymus and bone marrow, respectively. However, there has long been a belief that the immune system must have peripheral mechanisms in place to deal with immune cells that 'escape' central tolerance. For almost 40 years, immunologists have postulated the existence of suppressor T cells that police the immune system to avert unwanted immune responses 1-3 . However, that phenomenology was cast into doubt as various labs presented unique, hard-to-reproduce systems, each with complexities and idiosyncrasies that raised credibility issues. This situation was not unlike the early years of cytokine biology, during which dozens of activities were found in sera and cell supernatants without consistent molecular or biochemical 'signatures'. Fortunately, as biochemistry and the molecular biology revolution rescued the field of cytokine biology by identifying genes and biochemical structures tied to the varied biologic activities, the identification of a constellation of cell surface, transcriptional and biochemical markers that uniquely mark 'regulatory' T cells (T reg cells) has made possible a rebirth of the suppressor T cell field over the past decade.The realization that T reg cells have a unique surface expression profile incorporating CD25, CD62L and specific CD45 isoforms 4-6 , together with the identification of the T reg cellspecific transcription factor Foxp3, catapulted T reg cells from a rare CD4 + T cell subset to

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“…Полученные результаты говорят о лектин-зависимом меха-низме кросс-регуляции между отдельными суб-популяциями Тh-лимфоцитов. Применение рекомбинантного галектина-1 in vivo приводит к снижению количества Th1-клеток и увеличе-нию продукции IL-4 и IL-10 CD4 + Т-клетками [5,41,65]. Разнонаправленное действие галек-тина-1 на отдельные субпопуляции хелперных Т-лимфоцитов объясняется тем, что Тh1-и Тh17-дифференцированные клетки экспрессируют Галектин-1: роль в формировании 2012, Т.…”

Section: Cd8unclassified

“…Активационные сигналы, действующие на В-лимфоциты на периферии, вызывают апре-гуляцию галектина-1 [72]. Далее данный лектин способствует дифференцировке активированных В-клеток в плазматические клетки, секретирую-щие антитела [65]. Недавно было показано, что усиленная экспрессия галектина-1 может спо-собствовать гибели В-клеток памяти [61], таким образом подтвердив роль галектина-1 в поддер-жании фенотипа плазматических клеток.…”

Section: Cd8unclassified

Galectin-1 and Its Role in Development of Innate and Adaptive Immunity

Yakushina¹,

Васильева²,

Рязанцева³

et al. 2014

Med. immunol.

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Общие данные о галектине-1, как представите-ле семейства галектиновБыстрота и информативность, с которой рас-ширяются наши представления о регуляции иммунологического гомеостаза в норме и при различной патологии, ярко иллюстрируется Галектин-1: роль в формировании оСоБенноСтеЙ вроЖДенноГо и ПриоБретенноГо иммУнитета Якушина В.Д., Васильева О.А., Рязанцева Н.В., Новицкий В.В., Савельева О.Е., Прохоренко Т.С., Старикова Е.Г., Зима А.П. ГБОУ ВПО Сибирский государственный медицинский университет Минздравсоцразвития России, г. ТомскРезюме. Галектины -это β-галактозид-связывающие белки, объединенные в одно семейство со-гласно гомологии их углевод-распознающего домена. Данные лектины связываются с гликанами клеточной поверхности и экстрацеллюлярного матрикса, оказывая, таким образом, влияние на кле-точный цикл, адгезию, миграцию, пролиферацию и апоптоз. Кроме того, галектины способны дей-ствовать внутриклеточно и принимать участие, например, в сигнальной трансдукции, взаимодействуя с другими белками цитоплазмы и ядра. В регуляции функциональной активности клеток иммунной системы особое значение отводится галектину-1. Данный белок, являясь фактором кооперации им-мунокомпетентных клеток, способен модулировать иммунные реакции. В связи с этим, галектин-1 рассматривается в качестве возможного агента или мишени для разработки новых методов коррек-ции патологических процессов, связанных с дисбалансом клеток иммунной системы. В данной ста-тье приводится обзор работ посвященных изучению роли галектина-1 в формировании особенностей врожденного и приобретенного иммунитета. GALECTIN-1 AND ITS ROLE IN DEVELOPMENT OF INNATE AND ADAPTIVE IMMUNITYAbstract. Galectins comprise a family of β-galactoside-binding animal proteins, which are defined by common homologies of their carbohydrate-recognizing domaine (affinity for poly-N-acetyllactosamine). These lectins bind to cell surface glycans and extracellular matrix, thus influencing various cellular events, including cell cycle, adhesion, migration, proliferation and apoptosis. Moreover, galectins are able to exert intracellular effects, and participate, e.g., in signal transduction, by interacting with other nuclear and cytoplasmic proteins. Galectin-1 is considered to play a special role in functional regulation of immune cell activity. Thus protein is a factor of immunocompetent cell cooperation, thus being able to modulate immune reactions. In this respect, galectin-1 is considered as a potential agent or a target for new methods aimed to correct pathological processes associated with imbalance of immune system. This article provides an overview of works devoted to a possible role of galectin-1 in development of typical features of innate and adaptive immunity.

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O-Glycosylation Regulates LNCaP Prostate Cancer Cell Susceptibility to Apoptosis Induced by Galectin-1

Cited by 79 publications

References 44 publications

Differential Roles of Galectin-1 and Galectin-3 in Regulating Leukocyte Viability and Cytokine Secretion

Differential Roles of Galectin-1 and Galectin-3 in Regulating Leukocyte Viability and Cytokine Secretion

The Foxp3+ regulatory T cell: a jack of all trades, master of regulation

Galectin-1 and Its Role in Development of Innate and Adaptive Immunity

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