Galectin-1 Expression in CD8+ T Lymphocytes Controls Inflammation in Contact Hypersensitivity

Castillo-González, Raquel; Cibrián, Danay; Fernández‐Gallego, Nieves; Ramírez-Huesca, Marta; Sáiz, María Laura; Navarro, M.; Fresno, Manuel; Fuente, Hortensia de la; Sánchez-Madrid, Francisco

doi:10.1016/j.jid.2020.10.020

Cited by 10 publications

(6 citation statements)

References 34 publications

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“…Indeed, lymphocytes with higher levels of galectin-1 show lower cytotoxic effector capacity within a tumor contexture [190]. Experimental data also support that the intrinsic galectin-1 in T lymphocytes have major regulatory functions in other models of T cell immunity: infections, allergic contact dermatitis, and autoimmunity [188,189,259,260]. Aside from direct regulation of T cell function, galectin-1 may also control lymphocyte behavior through the participation of other cells.…”

Section: Galectin Functions Inside the Tumormentioning

confidence: 76%

Unraveling How Tumor-Derived Galectins Contribute to Anti-Cancer Immunity Failure

Laderach

Compagno

2021

Cancers

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Current data indicates that anti-tumor T cell-mediated immunity correlates with a better prognosis in cancer patients. However, it has widely been demonstrated that tumor cells negatively manage immune attack by activating several immune-suppressive mechanisms. It is, therefore, essential to fully understand how lymphocytes are activated in a tumor microenvironment and, above all, how to prevent these cells from becoming dysfunctional. Tumors produce galectins-1, -3, -7, -8, and -9 as one of the major molecular mechanisms to evade immune control of tumor development. These galectins impact different steps in the establishment of the anti-tumor immune responses. Here, we carry out a critical dissection on the mechanisms through which tumor-derived galectins can influence the production and the functionality of anti-tumor T lymphocytes. This knowledge may help us design more effective immunotherapies to treat human cancers.

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Section: Galectin Functions Inside the Tumormentioning

confidence: 76%

Unraveling How Tumor-Derived Galectins Contribute to Anti-Cancer Immunity Failure

Laderach

Compagno

2021

Cancers

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“…Aalinkeel et al ( 43 ) identified that galectin-1 can suppress the inflammation response of microglial cells. Castillo-González et al ( 44 ) found that deficient of galectin-1 resulted in increased infiltration of CD8 + T cells and neutrophils in the skin of mice. Thus galectin-1 can attenuate the activation of immune cells, regulate the oxidative stress and inflammation, and eventually ameliorate the I/R injury.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of galectin‑1 on cerebral ischemia/reperfusion injury by regulating oxidative stress

Zhao,

Zhu,

et al. 2024

Exp Ther Med

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Oxidative stress contributes to the pathology of cerebral ischemia/reperfusion (I/R) injury. Galectin-1 has shown an anti-oxidative stress effect. The present study investigated whether this anti-oxidative stress effect can account for the neuroprotective actions of galectin-1 induced by cerebral I/R injury. A cerebral I/R injury model was created in C57Bl/6 mice by transient occlusion of the middle cerebral artery, after which the mice were treated with galectin-1 for 3 days. Infarct volumes were measured. A rotarod test and neurological deficit score assessment was performed to evaluate the neurological deficits. Oxidative stress was evaluated by measuring the levels of reactive oxygen species (ROS) and lipid peroxidation malondialdehyde (MDA), while the anti-oxidative stress status was assessed by measuring molecules such as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidation enzyme (GSH-Px) in the ischemic cerebral hemisphere of mice. The inflammatory cytokines, including Interleukin 1 (IL-1), IL-6 and tumor necrosis factor alpha (TNF-α) were measured, and the expression of microglia was evaluated by immunohistochemistry in the ischemic cerebral hemisphere of mice. Galectin-1 treatment ameliorated neurological deficits and reduced infarct volumes in the mice model with cerebral I/R injury. Moreover, it was demonstrated that galectin-1 can significantly alleviate cerebral I/R injury in the ischemic cerebral hemisphere by decreasing the production of ROS and MDA, but increasing the production of CAT, SOD and GSH-Px. Galectin-1 treatment decreased microglia expression, and IL-1, IL-6 and TNF-α levels in the ischemic cerebral hemisphere of mice. Galectin-1 could improve the outcome of cerebral I/R injury by alleviating oxidative stress. Moreover, the neuroprotective effect of galectin-1 in cerebral ischemia could be related to its anti-oxidative stress effect.

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“…On the transcriptional level, a noteworthy phenomenon was that up-regulated genes of APC GAL-1−/− were mainly related to immune responses, including the immune system’s responses to bacteria and viruses. According to previous studies, GAL-1 has a powerful immunosuppressive effect by inhibiting T cell proliferation or inducing T cell apoptosis [ 46 – 48 ]. Scar formation in the immune process of wound injury plays a key role in preventing regeneration.…”

Section: Discussionmentioning

confidence: 99%

Galectin-1 promotes angiogenesis and chondrogenesis during antler regeneration

Shi

Wei

et al. 2023

Cell Mol Biol Lett

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Background Deer antlers are the only known mammalian structure that undergoes full regeneration. In addition, it is peculiar because when growing, it contains vascularized cartilage. The differentiation of antler stem cells (ASCs) into chondrocytes while inducing endochondral extension of blood vessels is necessary to form antler vascularized cartilage. Therefore, antlers provide an unparalleled opportunity to investigate chondrogenesis, angiogenesis, and regenerative medicine. A study found that Galectin-1 (GAL-1), which can be used as a marker in some tumors, is highly expressed in ASCs. This intrigued us to investigate what role GAL-1 could play in antler regeneration. Methods We measured the expression level of GAL-1 in antler tissues and cells by immunohistochemistry, WB and QPCR. We constructed antlerogenic periosteal cells (APCs, one cell type of ASCs) with the GAL-1 gene knocked out (APCGAL-1−/−) using CRISPR-CAS9 gene editing system. The effect of GAL-1 on angiogenesis was determined by stimulating human umbilical vein endothelial cells (HUVECs) using APCGAL-1−/− conditioned medium or adding exogenous deer GAL-1 protein. The effect of APCGAL-1−/− on chondrogenic differentiation was evaluated compared with the APCs under micro-mass culture. The gene expression pattern of APCGAL-1−/− was analyzed by transcriptome sequencing. Results Immunohistochemistry revealed that GAL-1 was widely expressed in the antlerogenic periosteum (AP), pedicle periosteum (PP) and antler growth center. Western blot and qRT-PCR analysis using deer cell lines further supports this result. The proliferation, migration, and tube formation assays of human umbilical vein endothelial cells (HUVECs) showed that the proangiogenic activity of APCGAL-1−/− medium was significantly decreased (P < 0.05) compared with the APCs medium. The proangiogenic activity of deer GAL-1 protein was further confirmed by adding exogenous deer GAL-1 protein (P < 0.05). The chondrogenic differentiation ability of APCGAL-1−/− was impeded under micro-mass culture. The terms of GO and KEGG enrichment of the differentially expressed genes (DEGs) of APCGAL-1−/− showed that down-regulated expression of pathways associated with deer antler angiogenesis, osteogenesis and stem cell pluripotency, such as the PI3K-AKT signaling pathway, signaling pathways regulating pluripotency of stem cells and TGF-β signaling pathway. Conclusions Deer GAL-1, has strong angiogenic activity, is widely and highly expressed in deer antler. The APCs can induce angiogenesis by secreting GAL-1. The knockout of GAL-1 gene of APCs damaged its ability to induce angiogenesis and differentiate into chondrocytes. This ability is crucial to the formation of deer antler vascularized cartilage. Moreover, Deer antlers offer a unique model to explore explore how angiogenesis at high levels of GAL-1 expression can be elegantly regulated without becoming cancerous. Graphical Abstract

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Galectin-1 Expression in CD8+ T Lymphocytes Controls Inflammation in Contact Hypersensitivity

Cited by 10 publications

References 34 publications

Unraveling How Tumor-Derived Galectins Contribute to Anti-Cancer Immunity Failure

Unraveling How Tumor-Derived Galectins Contribute to Anti-Cancer Immunity Failure

Neuroprotective effects of galectin‑1 on cerebral ischemia/reperfusion injury by regulating oxidative stress

Galectin-1 promotes angiogenesis and chondrogenesis during antler regeneration

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