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Search results for: CD1D

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#38622654   2024/04/15 To Up

Immunotherapy with an antibody against CD1d modulates neuroinflammation in an α-synuclein transgenic model of Lewy body like disease.

The neuroinflammatory process in synucleinopathies of the aging population such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB) involves microglial activation as well as infiltration of the CNS by T cells and natural killer T cells (NKTs). To evaluate the potential of targeting NKT cells to modulate neuroinflammation, we treated α-syn transgenic (tg) mice (e.g.: Thy1 promoter line 61) with an antibody against CD1d, which is a glycoprotein expressed in antigen presenting cells (APCs). CD1d-presented lipid antigens activate NKT cells through the interaction with T cell receptor in NKTs, resulting in the production of cytokines. Thus, we hypothesized that blocking the APC-NKT interaction with an anti-CD1d antibody might reduce neuroinflammation and neurodegeneration in models of DLB/PD. Treatment with the anti-CD1d antibody did not have effects on CD3 (T cells), slightly decreased CD4 and increased CD8 lymphocytes in the mice. Moreover, double labeling studies showed that compared to control (IgG) treated α-syn tg mice, treatment with anti-CD1d decreased numbers of CD3/interferon γ (IFN γ)-positive cells, consistent with NKTs. Further double labeling studies showed that CD1d-positive cells co-localized with the astrocytes marker GFAP and that anti-CD1d antibody reduced this effect. While in control α-syn tg mice CD3 positive cells were near astrocytes, this was modified by the treatment with the CD1d antibody. By qPCR, levels of IFN γ, CCL4, and interleukin-6 were increased in the IgG treated α-syn tg mice. Treatment with CD1d antibody blunted this cytokine response that was associated with reduced astrocytosis and microgliosis in the CNS of the α-syn tg mice treated with CD1d antibody. Flow cytometric analysis of immune cells in α-syn tg mice revealed that CD1d-tet + T cells were also increased in the spleen of α-syn tg mice, which treatment with the CD1d antibody reduced. Reduced neuroinflammation in the anti-CD1d-treated α-syn tg mice was associated with amelioration of neurodegenerative pathology. These results suggest that reducing infiltration of NKT cells with an antibody against CD1d might be a potential therapeutical approach for DLB/PD.
Michiyo Iba, Somin Kwon, Changyoun Kim, Marcell Szabo, Liam Horan-Portelance, Maria Lopez-Ocasio, Pradeep Dagur, Cassia Overk, Robert A Rissman, Eliezer Masliah

1924 related Products with: Immunotherapy with an antibody against CD1d modulates neuroinflammation in an α-synuclein transgenic model of Lewy body like disease.

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#38586879   2024/04/08 To Up

Ox-LDL-induced CD80 macrophages expand pro-atherosclerotic NKT cells via CD1d in atherosclerotic mice and hyperlipidemic patients.

Atherosclerosis is an inflammatory disease of blood vessels involving the immune system. Natural killer T (NKT) cells, as crucial components of the innate and acquired immune systems, play critical roles in the development of atherosclerosis. However, the mechanism and clinical relevance of NKT cells in early atherosclerosis are largely unclear. Our findings demonstrated that there were higher populations of NKT cells and interferon gamma (IFN-γ)-producing NKT cells in the peripheral blood of patients with hyperlipidemia and in the aorta, blood, spleen, and bone marrow of early atherosclerotic mice compared to control groups. Moreover, we discovered that the infiltration of M1 macrophages and CD1d expression on M1 macrophages in atherosclerotic mice climbed remarkably. CD1d expression increased in M1 macrophages stimulated by oxidized low-density lipoprotein (ox-LDL) and . co-culture of macrophages with NKT cells revealed that ox-LDL-induced M1 macrophages presented lipid antigen alpha-galactosylceramide (α-Galcer) to NKT cells via CD1d, enabling NKT cells to express more IFN-γ. Furthermore, a greater proportion of CD1dmonocytes and CD1dM1 monocytes were found in peripheral blood of hyperlipidemic patients compared with that of healthy donors. Positive correlations were found between CD1d M1 monocytes and NKT cells or IFN-γ NKT cells in hyperlipidemic patients. Our findings illustrate that M1 macrophages stimulate NKT cells to secret IFN-γ via CD1d presenting α-Galcer, which may accelerate the progression of early atherosclerosis. Inhibiting lipid antigen presentation by M1 macrophages to NKT cells may be a promising immune target for the treatment of early atherosclerosis.
Yin Wang, Yao Zou, Qingsong Jiang, Wenming Li, Xinyu Chai, Tingrui Zhao, Siyi Liu, Zhiyi Yuan, Chao Yu, Tingting Wang

2113 related Products with: Ox-LDL-induced CD80 macrophages expand pro-atherosclerotic NKT cells via CD1d in atherosclerotic mice and hyperlipidemic patients.

400 ug10 rxns100 ul96 assays100ug1 mg1.00 flask1x10e7 cells96T100ug/vial400 ug100 ug/vial

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#38579449   2024/04/04 To Up

CD1 molecules: Beyond antigen presentation.

CD1 molecules are well known for their role in binding and presenting lipid antigens to mediate the activation of CD1-restricted T cells. However, much less appreciated is the fact that CD1 molecules can have additional "unconventional" roles which impact the activation and functions of CD1-expressing cells, ultimately controlling tissue homeostasis as well as the progression of inflammatory and infectious diseases. Some of these roles are mediated by so-called reverse signalling, by which crosslinking of CD1 molecules at the cell surface initiates intracellular signalling. On the other hand, CD1 molecules can also control metabolic and inflammatory pathways in CD1-expressing cells through cell-intrinsic mechanisms independent of CD1 ligation. Here, we review the evidence for "unconventional" functions of CD1 molecules and the outcomes of such roles for health and disease.
Lauren Evans, Patricia Barral

2996 related Products with: CD1 molecules: Beyond antigen presentation.

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#38557824   2024/04/01 To Up

Recent advances regarding the potential roles of invariant natural killer T cells in cardiovascular diseases with immunological and inflammatory backgrounds.

Invariant natural killer T (iNKT) cells, which bear αβ-type T cell antigen-receptors, recognize glycolipid antigens in a cluster of differentiation 1d (CD1d)-restricted manner. Regarding these cells, the unique modes of thymic selection and maturation elucidate innateness, irrespective of them also being members of the adaptive immune system as a T cell. iNKT cells develop and differentiate into NKT1 [interferon γ (IFN-γγ-producing], NKT2 [interleukin 4 (IL-4)/IL-13-producing], or NKT17 (IL-17-producing) subsets in the thymus. After egress, NKT10 (IL-10-producing), follicular helper NKT (NKTfh; IL-21-producing), and regulatory NKT (NKTreg) subsets emerge following stimulation in the periphery. Moreover, iNKT cells have been shown to possess several physiological or pathological roles. iNKT cells exhibit dual alleviating or aggravating roles in experimentally induced immune and/or inflammatory diseases in mice. These findings indicate that the modulation of iNKT cells can be employed for therapeutic use or prevention of human diseases. In this review, we discuss the potential roles of iNKT cells in the development of immune/inflammatory diseases of the cardiovascular system, with emphasis on atherosclerosis, aortic aneurysms, and cardiac remodeling.
Kazuya Iwabuchi, Masashi Satoh, Kazuhisa Yoshino, Naoki Ishimori

1175 related Products with: Recent advances regarding the potential roles of invariant natural killer T cells in cardiovascular diseases with immunological and inflammatory backgrounds.

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#38536025   2024/03/27 To Up

Correction: DX5/CD49b-Positive T Cells Are Not Synonymous with CD1d-Dependent NKT Cells.

Pellicci, D. G., K. J. L. Hammond, J. Coquet, K. Kyparissoudis, A. G. Brooks, K. Kedzierska, R. Keating, S. Turner, S. Berzins, M. J. Smyth, and D. I. Godfrey. 2005. DX5/CD49b-positive T cells are not synonymous with CD1d-dependent NKT cells. J. Immunol. 175: 4416-4425. Fig. 2A of this article contains flow cytometry comparing C57BL/6 WT mice and CD1d-/- mice for αβTCR versus DX5 or αβTCR versus CD49b staining in mouse thymus, spleen, liver, bone marrow, and peripheral lymph nodes (PLNs). Abs for DX5 and CD49b bind the same molecule (integrin α2 or CD49b). The FACS plot representing αβTCR versus DX5 for thymus and bone marrow in CD1d-/- mice inadvertently showed αβTCR versus CD49b from CD1d-/- mice and thus these plots were unintentionally duplicated during the figure generation. Importantly, the data presented in the graphs of Fig. 2A were correct as originally published. The correct version of Fig. 2A is now shown below. The conclusions for this manuscript remain unchanged.The figure legend was correct as originally published. The legend for Fig. 2A is shown below for reference.
Daniel G Pellicci, Kirsten J L Hammond, Jonathan Coquet, Konstantinos Kyparissoudis, Andrew G Brooks, Katherine Kedzierska, Rachael Keating, Stephen Turner, Stuart Berzins, Mark J Smyth, Dale I Godfrey

1561 related Products with: Correction: DX5/CD49b-Positive T Cells Are Not Synonymous with CD1d-Dependent NKT Cells.

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#38484172   2024/03/14 To Up

Integrating Tertiary Lymphoid Structure-Associated Genes into Computational Models to Evaluate Prognostication and Immune Infiltration in Pancreatic Cancer.

Pancreatic ductal adenocarcinoma (PDAC) is characterized by poor response to all therapeutic modalities and dismal prognosis. The presence of tertiary lymphoid structures (TLSs) in various solid cancers is of crucial prognostic significance, highlighting the intricate interplay between the tumor microenvironment and immune cells aggregation. However, the extent to which TLS and immune status affect PDAC prognosis remains incompletely understood. Here, we sought to unveil the unique properties of TLS in PDAC by leveraging both single-cell and bulk transcriptomics, and culminating in a risk model that predicts clinical outcomes. We used TLS score based on 12 genes (CCL2, CCL3, CCL4, CCL5, CCL8, CCL18, CCL19, CCL21, CXCL9, CXCL10, CXCL11 and CXCL13) and 9 genes (PTGDS, RBP5, EIF1AY, CETP, SKAP1, LAT, CCR6, CD1D and CD79B) signature, respectively, and examined their distribution in cell clusters of single-cell data from PDAC samples. The markers involved in these clusters were selected to develop a prognostic model using The Cancer Genome Atlas Program (TCGA) database as the training cohort and Gene Expression Omnibus (GEO) database as the validation cohort. Further we compared the immune infiltration, drug sensitivity, enriched and differentially expressed genes between the high-risk and low-risk groups in our model. Therefore, we established a risk model that has significant implications for the prognostic assessment of PADC patients with remarkable differences in immune infiltration and chemo-sensitivity between the low-risk and high-risk groups. And this paradigm established by TLS-related cell marker genes provides a prognostic prediction and a panel of novel therapeutic targets for exploring potential immunotherapy.
Ying Ma, Xuesong Li, Jin Zhang, Xiangqin Zhao, Yi Lu, Guangcong Shen, Guowen Wang, Hong Liu, Jihui Hao

1005 related Products with: Integrating Tertiary Lymphoid Structure-Associated Genes into Computational Models to Evaluate Prognostication and Immune Infiltration in Pancreatic Cancer.



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#38477945   2024/03/13 To Up

A Humanized Mouse Model Coupled with Computational Analysis Identifies Potent Glycolipid Agonist of Invariant NKT Cells.

Invariant natural killer T (iNKT) cells play an important role in many innate and adaptive immune responses, with potential applications in cancer immunotherapy. The glycolipid KRN7000, an α-galactosylceramide, potently activates iNKT cells but has shown limited anticancer effects in human clinical trials conducted so far. In spite of almost three decades of structure-activity relationship studies, no alternative glycolipid has yet emerged as a superior clinical candidate. One reason for the slow progress in this area is that standard mouse models do not accurately reflect the specific ligand recognition by human iNKT cells and their requirements for activation. Here we evaluated a series of KRN7000 analogues using a recently developed humanized mouse model that expresses a human αTCR chain sequence and human CD1d. In this process, a more stimulatory, previously reported but largely overlooked glycolipid was identified, and its activity was probed and rationalized via molecular simulations.
Noemi A Saavedra-Avila, Natalia B Pigni, Donald R Caldwell, Florencia Chena-Becerra, Jose Intano, Tony W Ng, Divya Chennamadhavuni, Steven A Porcelli, José A Gascón, Amy R Howell

2323 related Products with: A Humanized Mouse Model Coupled with Computational Analysis Identifies Potent Glycolipid Agonist of Invariant NKT Cells.

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#38460658   2024/03/07 To Up

Role of sulfatide-reactive vNKT cells in promoting lung Treg cells via dendritic cell modulation in asthma models.

Our previous studies have showed that sulfatide-reactive type II NKT (i.e. variant NKT, vNKT) cells inhibit the immunogenic maturation during the development of mature lung dendritic cells (LDCs), leading todeclined allergic airway inflammation in asthma. Nonetheless, the specific immunoregulatory roles of vNKT cells in LDC-mediated Th2 cell responses remain incompletely understood. Herein, we found that administration of sulfatide facilitated the generation of CD4FoxP3 regulatory T (Treg) cells in the lungs of wild-type mice, but not in CD1d and Jα18 mice, after ovalbumin or house dust mite exposure. This finding implies that the enhancement of lung Treg cells by sulfatide requires vNKT cells, which dependent on invariant NKT (iNKT) cells. Furthermore, the CD4FoxP3 Treg cells induced by sulfatide-reactive vNKT cells were found to be associated with PD-L1 molecules expressed on LDCs, and this association was dependent on iNKT cells. Collectively, our findings suggest that in asthma-mimicking murine models, sulfatide-reactive vNKT cells facilitate the generation of lung Treg cells through inducing tolerogenic properties in LDCs, and this process is dependent on the presence of lung iNKT cells. These results may provide a potential therapeutic approach to treat allergic asthma.
Haiyang Ni, Qibin Lin, Jieying Zhong, Shaoding Gan, Hong Cheng, Yi Huang, Xuhong Ding, Hongying Yu, Yaqing Xu, Hanxiang Nie

1270 related Products with: Role of sulfatide-reactive vNKT cells in promoting lung Treg cells via dendritic cell modulation in asthma models.

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#38440725   2024/02/19 To Up

Insights into the heterogeneity of iNKT cells: tissue-resident and circulating subsets shaped by local microenvironmental cues.

Invariant natural killer T (iNKT) cells are a distinct subpopulation of innate-like T lymphocytes. They are characterized by semi-invariant T cell receptors (TCRs) that recognize both self and foreign lipid antigens presented by CD1d, a non-polymorphic MHC class I-like molecule. iNKT cells play a critical role in stimulating innate and adaptive immune responses, providing an effective defense against infections and cancers, while also contributing to chronic inflammation. The functions of iNKT cells are specific to their location, ranging from lymphoid to non-lymphoid tissues, such as the thymus, lung, liver, intestine, and adipose tissue. This review aims to provide insights into the heterogeneity of development and function in iNKT cells. First, we will review the expression of master transcription factors that define subsets of iNKT cells and their production of effector molecules such as cytokines and granzymes. In this article, we describe the gene expression profiles contributing to the kinetics, distribution, and cytotoxicity of iNKT cells across different tissue types. We also review the impact of cytokine production in distinct immune microenvironments on iNKT cell heterogeneity, highlighting a recently identified circulating iNKT cell subset. Additionally, we explore the potential of exploiting iNKT cell heterogeneity to create potent immunotherapies for human cancers in the future.
Guangwei Cui, Shinya Abe, Ryoma Kato, Koichi Ikuta

2314 related Products with: Insights into the heterogeneity of iNKT cells: tissue-resident and circulating subsets shaped by local microenvironmental cues.

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#38438948   2023/10/28 To Up

CD1d protects against hepatocyte apoptosis in non-alcoholic steatohepatitis.

Hepatocyte apoptosis, a well-defined form of cell death in non-alcoholic steatohepatitis (NASH), is considered the primary cause of liver inflammation and fibrosis. However, the mechanisms underlying the regulation of hepatocyte apoptosis in NASH remain largely unclear. We explored the anti-apoptotic effect of hepatocyte CD1d in NASH.
Zhigang Lei, Jiaojiao Yu, Yu Wu, Junyao Shen, Shibo Lin, Weijie Xue, Chenxu Mao, Rui Tang, Haoran Sun, Xin Qi, Xiaohong Wang, Lei Xu, Chuan Wei, Xiaowei Wang, Hongbing Chen, Ping Hao, Wen Yin, Jifeng Zhu, Yalin Li, Yi Wu, Shouguo Liu, Hui Liang, Xiaojun Chen, Chuan Su, Sha Zhou

1880 related Products with: CD1d protects against hepatocyte apoptosis in non-alcoholic steatohepatitis.

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