scholarly journals Natural Killer T Cells in Various Mouse Models of Hepatitis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Jun Guan ◽  
Gang Wang ◽  
Qin Yang ◽  
Chao Chen ◽  
Jingwen Deng ◽  
...  
Keyword(s):  
Natural Killer ◽  
Mouse Models ◽  
Fas Ligand ◽  
Basic Research ◽  
Neutrophil Infiltration ◽  
Nkt Cells ◽  
Liver Injuries ◽  
Integral Role ◽  
Natural Killer T

Natural killer T (NKT) cells are a key component of innate immunity. Importantly, a growing body of evidence indicates that NKT cells play an integral role in various acute and chronic liver injuries. NKT cells participate in the progression of an injury through the secretion of cytokines, which promote neutrophil infiltration and enhance Fas ligand (FasL) and granzyme-mediated NKT cytotoxic activity. Therefore, examining the role of NKT cells in hepatic disease is critical for a comprehensive understanding of disease pathogenesis and may provide insight into novel approaches for treatment. For more than a century, mouse models that imitate the physiopathological conditions of human disease have served as a critical tool in biological and medical basic research, including studies of liver disease. Here, we review the role of NKT cells in various mouse models of hepatitis.

Participatory role of natural killer and natural killer T cells in atherosclerosis: lessons learned from in vivo mouse studiesThis paper is one of a selection of papers published in this Special Issue, entitled Young Investigator's Forum.

2006 ◽  
Vol 84 (1) ◽  
pp. 67-75 ◽  
Author(s):  
Stewart C. Whitman ◽  
Tanya A. Ramsamy
Keyword(s):  
Natural Killer ◽  
Complex Disease ◽  
Immune Cell ◽  
Disease Process ◽  
Density Lipoprotein ◽  
Nkt Cells ◽  
Lessons Learned ◽  
Natural Killer T

Atherosclerosis is a multifactor, highly complex disease with numerous aetiologies that work synergistically to promote lesion development. One of the emerging components that drive the development of both early- and late-stage atherosclerotic lesions is the participation of both the innate and acquired immune systems. In both humans and animal models of atherosclerosis, the most prominent cells that infiltrate evolving lesions are macrophages and T lymphocytes. The functional loss of either of these cell types reduces the extent of atherosclerosis in mice that were rendered susceptible to the disease by deficiency of either apolipoprotein E or the LDL (low density lipoprotein) receptor. In addition to these major immune cell participants, a number of less prominent leukocyte populations that can modulate the atherogenic process are also involved. This review will focus on the participatory role of two “less prominent” immune components, namely natural killer (NK) cells and natural killer T (NKT) cells. Although this review will highlight the fact that both NK and NKT cells are not sufficient for causing the disease, the roles played by both these cells types are becoming increasingly important in understanding the complexity of this disease process.

scholarly journals Role of Natural Killer T (NKT) Cells in Type II Diabetes-Induced Vascular Injuries

2018 ◽  
Vol 24 ◽  
pp. 8322-8332 ◽  
Author(s):  
Xiaohong Lv ◽  
Yun Gao ◽  
Tantan Dong ◽  
Libo Yang
Keyword(s):  
Natural Killer ◽  
Type Ii Diabetes ◽  
Nkt Cells ◽  
Vascular Injuries ◽  
Type Ii ◽  
Natural Killer T

scholarly journals Infections, Reactions of Natural Killer T Cells and Natural Killer Cells, and Kidney Injury

2022 ◽  
Vol 23 (1) ◽  
pp. 479
Author(s):  
Takahiro Uchida ◽  
Shuhji Seki ◽  
Takashi Oda
Keyword(s):  
T Cells ◽  
Nk Cells ◽  
Natural Killer ◽  
Fas Ligand ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Kidney Injury ◽  
Nkt Cells ◽  
Renal Diseases ◽  
Natural Killer T

Natural killer T (NKT) cells and NK cells are representative innate immune cells that perform antitumor and antimicrobial functions. The involvement of these cells in various renal diseases, including acute kidney injury (AKI), has recently become evident. Murine NKT cells are activated and cause AKI in response to various stimuli, such as their specific ligand, cytokines, and bacterial components. Both renal vascular endothelial cell injury (via the perforin-mediated pathway) and tubular epithelial cell injury (via the tumor necrosis factor-alpha/Fas ligand pathway) are independently involved in the pathogenesis of AKI. NK cells complement the functions of NKT cells, thereby contributing to the development of infection-associated AKI. Human CD56+ T cells, which are a functional counterpart of murine NKT cells, as well as a subpopulation of CD56+ NK cells, strongly damage intrinsic renal cells in vitro upon their activation, possibly through mechanisms similar to those in mice. These cells are also thought to be involved in the acute exacerbation of pre-existing glomerulonephritis triggered by infection in humans, and their roles in sepsis-associated AKI are currently under investigation. In this review, we will provide an overview of the recent advances in the understanding of the association among infections, NKT and NK cells, and kidney injury, which is much more profound than previously considered. The important role of liver macrophages in the activation of NKT cells will also be introduced.

scholarly journals Identification and Simian Immunodeficiency Virus Infection of CD1d-Restricted Macaque Natural Killer T Cells

2003 ◽  
Vol 77 (14) ◽  
pp. 8153-8158 ◽  
Author(s):  
Alison Motsinger ◽  
Agnes Azimzadeh ◽  
Aleksandar K. Stanic ◽  
R. Paul Johnson ◽  
Luc Van Kaer ◽  
...  
Keyword(s):  
T Cells ◽  
Natural Killer ◽  
Simian Immunodeficiency Virus ◽  
Cell Receptor ◽  
Nkt Cells ◽  
Immunodeficiency Virus ◽  
Siv Infection ◽  
Hiv 1 ◽  
Natural Killer T

ABSTRACT Natural killer T (NKT) cells express a highly conserved T-cell receptor (TCR) and recognize glycolipids in the context of CD1d molecules. We recently demonstrated that CD4+ NKT cells are highly susceptible to human immunodeficiency virus type 1 (HIV-1) infection and are selectively depleted in HIV-infected individuals. Here, we identified macaque NKT cells using CD1d tetramers and human Vα24 antibodies. Similar to human NKT cells, α-galactosylceramide (α-GalCer)-pulsed dendritic cells activate and expand macaque NKT cells. Upon restimulation with α-GalCer-pulsed CD1d+ cells, macaque NKT cells secreted high levels of cytokines, a characteristic of these T cells. Remarkably, the majority of resting and activated macaque NKT cells expressed CD8, and a smaller portion expressed CD4. Macaque NKT cells also expressed the HIV-1/simian immunodeficiency virus (SIV) coreceptor CCR5, and the CD4+ subset was susceptible to SIV infection. Identification of macaque NKT cells has major implications for delineating the role of these cells in nonhuman primate disease models of HIV as well as other pathological conditions, such as allograft rejection and autoimmunity.

scholarly journals Combined proinflammatory cytokine and cognate activation of invariant natural killer T cells enhances anti-DNA antibody responses

2020 ◽  
Vol 117 (16) ◽  
pp. 9054-9063 ◽  
Author(s):  
Saikiran K. Sedimbi ◽  
Thomas Hägglöf ◽  
Manasa G. Garimella ◽  
Shan Wang ◽  
Amanda Duhlin ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Natural Killer ◽  
Chronic Inflammation ◽  
Cell Activation ◽  
Fas Ligand ◽  
Nkt Cells ◽  
Autoreactive B Cells ◽  
Invariant Natural Killer ◽  
Natural Killer T

Invariant natural killer T (iNKT) cells serve as early rapid responders in the innate immune response to self-derived autoantigens and pathogen-derived danger signals and antigens. iNKT cells can serve both as helpers for effector B cells and negatively regulate autoreactive B cells. Specifically, iNKT cells drive B cell proliferation, class switch, and antibody production to induce primary antigen-specific immune responses. On the other hand, inflammasome-mediated activation drives accumulation of neutrophils, which license iNKT cells to negatively regulate autoreactive B cells via Fas ligand (FasL). This positions iNKT cells at an apex to support or inhibit B cell responses in inflammation. However, it is unknown which effector mechanism dominates in the face of cognate glycolipid activation during chronic inflammation, as might result from glycolipid vaccination or infection during chronic autoimmune disease. We stimulated iNKT cells by cognate glycolipid antigen α-galactosylceramide (αGalCer) and measured B cell activation during interleukin 18 (IL-18)-induced chronic inflammation. Moreover, glycolipid-activated iNKT cells increased the serum concentration of autoantibodies, frequency of germinal center (GC) B cells, and antigen-specific plasma cells induced during chronic IL-18–mediated inflammation, as compared with IL-18 alone. Further, activation of iNKT cells via cognate glycolipid during IL-18–mediated inflammation overrides the licensing function of neutrophils, instead inducing iNKT follicular helper (iNKTfh) cells that in turn promote autoimmunity. Thus, our data demonstrate that glycolipids which engage iNKT cells support antigen-specific B cell help during inflammasome-mediated inflammation.

scholarly journals Type I natural killer T cells suppress tumors caused by p53 loss in mice

Blood ◽  
2009 ◽  
Vol 113 (25) ◽  
pp. 6382-6385 ◽  
Author(s):  
Jeremy B. Swann ◽  
Adam P. Uldrich ◽  
Serani van Dommelen ◽  
Janelle Sharkey ◽  
William K. Murray ◽  
...  
Keyword(s):  
T Cells ◽  
Natural Killer ◽  
Immune Surveillance ◽  
Tumor Development ◽  
Natural Killer T Cells ◽  
Nkt Cells ◽  
Type I ◽  
Killer T Cells ◽  
Natural Killer T

Abstract CD1d-restricted T cells are considered to play a host protective effect in tumor immunity, yet the evidence for a role of natural killer T (NKT) cells in tumor immune surveillance has been weak and data from several tumor models has suggested that some (type II) CD1d-restricted T cells may also suppress some types of antitumor immune response. To substantiate an important role for CD1d-restricted T cells in host response to cancer, we have evaluated tumor development in p53+/− mice lacking either type I NKT cells (TCR Jα18−/−) or all CD1d-restricted T cells (CD1d−/−). Our findings support a key role for type I NKT cells in suppressing the onset of sarcomas and hematopoietic cancers caused by p53 loss but do not suggest that other CD1d-restricted T cells are critical in regulating the same tumor development.

The Role of Natural Killer T (NKT) Cells in the Pathogenesis of Type 1 Diabetes

2011 ◽  
Vol 7 (4) ◽  
pp. 278-283 ◽  
Author(s):  
Rita A. Gomez-Diaz ◽  
Mayra V. Aguilar ◽  
Elisa N. Meguro ◽  
Rocio H. Marquez ◽  
Eulalia G. Magana ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Natural Killer ◽  
Nkt Cells ◽  
Natural Killer T

scholarly journals Transcriptome and Function of Novel Immunosuppressive Autoreactive Invariant Natural Killer T Cells That Are Absent in Progressive Multiple Sclerosis

2021 ◽  
Vol 8 (6) ◽  
pp. e1065
Author(s):  
Belinda Carrión ◽  
Yawei Liu ◽  
Mahdieh Hadi ◽  
Jon Lundstrom ◽  
Jeppe Romme Christensen ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cells ◽  
Natural Killer ◽  
Protein Level ◽  
Fas Ligand ◽  
Nkt Cells ◽  
Tnf Receptor ◽  
Inkt Cells ◽  
Invariant Natural Killer ◽  
Natural Killer T

Background and ObjectiveThe aim of this study was to determine whether natural killer T (NKT) cells, including invariant (i) NKT cells, have clinical value in preventing the progression of multiple sclerosis (MS) by examining the mechanisms by which a distinct self-peptide induces a novel, protective invariant natural killer T cell (iNKT cell) subset.MethodsWe performed a transcriptomic and functional analysis of iNKT cells that were reactive to a human collagen type II self-peptide, hCII707-721, measuring differentially induced genes, cytokines, and suppressive capacity.ResultsWe report the first transcriptomic profile of human conventional vs novel hCII707-721–reactive iNKT cells. We determined that hCII707-721 induces protective iNKT cells that are found in the blood of healthy individuals but not progressive patients with MS (PMS). By transcriptomic analysis, we observed that hCII707-721 promotes their development and proliferation, favoring the splicing of full-length AKT serine/threonine kinase 1 (AKT1) and effector function of this unique lineage by upregulating tumor necrosis factor (TNF)-related genes. Furthermore, hCII707-721–reactive iNKT cells did not upregulate interferon (IFN)-γ, interleukin (IL)-4, IL-10, IL-13, or IL-17 by RNA-seq or at the protein level, unlike the response to the glycolipid alpha-galactosylceramide. hCII707-721–reactive iNKT cells increased TNFα only at the protein level and suppressed autologous-activated T cells through FAS-FAS ligand (FAS-FASL) and TNFα-TNF receptor I signaling but not TNF receptor II.DiscussionBased on their immunomodulatory properties, NKT cells have a potential value in the treatment of autoimmune diseases, such as MS. These significant findings suggest that endogenous peptide ligands can be used to expand iNKT cells, without causing a cytokine storm, constituting a potential immunotherapy for autoimmune conditions, including PMS.

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