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Article ; Online: Regulation of Tim-3 function by binding to phosphatidylserine.

Kane, Lawrence P

2021 Volume 478, Issue 22, Page(s) 3999–4004

Abstract: Tim-3 is a transmembrane protein that is highly expressed on subsets of chronically stimulated CD4+ helper and CD8+ cytotoxic T cells, with more transient expression during acute activation and infection. Tim-3 is also constitutively expressed by ... ...

Abstract	Tim-3 is a transmembrane protein that is highly expressed on subsets of chronically stimulated CD4+ helper and CD8+ cytotoxic T cells, with more transient expression during acute activation and infection. Tim-3 is also constitutively expressed by multiple types of myeloid cells. Like other TIM family members, Tim-3 can bind to phosphatidylserine displayed by apoptotic cells, and this interaction has been shown to mediate uptake of such cells by dendritic cells and cross-presentation of antigens to CD8+ T cells. In contrast, how the recognition of PS by Tim-3 might regulate the function of Tim-3+ T cells is not known. In their recent paper, Lemmon and colleagues demonstrate for the first time that recognition of PS by Tim-3 leads to enhanced T cell activation.
MeSH term(s)	Hepatitis A Virus Cellular Receptor 2/genetics ; Lymphocyte Activation ; Membrane Proteins/genetics ; Phagocytosis ; Phosphatidylserines
Chemical Substances	Hepatitis A Virus Cellular Receptor 2 ; Membrane Proteins ; Phosphatidylserines
Language	English
Publishing date	2021-12-21
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20210652
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Article ; Online: Tim-3 Is Not Required for Establishment of CD8+ T Cell Memory to Lymphocytic Choriomeningitis Virus.

Manandhar, Priyanka / Szymczak-Workman, Andrea L / Kane, Lawrence P

Journal of immunology (Baltimore, Md. : 1950)

2023 Volume 212, Issue 3, Page(s) 466–474

Abstract: Tim-3 is a transmembrane protein that is best known for being highly expressed on terminally exhausted CD8+ T cells associated with chronic infection and tumors, although its expression is not limited to those settings. Tim-3 is also expressed by CD8+ T ... ...

Abstract	Tim-3 is a transmembrane protein that is best known for being highly expressed on terminally exhausted CD8+ T cells associated with chronic infection and tumors, although its expression is not limited to those settings. Tim-3 is also expressed by CD8+ T cells during acute infection and by multiple other immune cell types, including CD4+ Th1 and regulatory T cells, dendritic cells, and mast cells. In this study, we investigated the role of Tim-3 signaling on CD8+ T cell memory using a Tim-3 conditional knockout mouse model and mice lacking the signaling portion of the Tim-3 cytoplasmic domain. Together, our results indicate that Tim-3 has at most a modest effect on the formation and function of CD8+ memory T cells.
MeSH term(s)	Animals ; Mice ; CD8-Positive T-Lymphocytes ; Hepatitis A Virus Cellular Receptor 2/genetics ; Hepatitis A Virus Cellular Receptor 2/metabolism ; Lymphocytic Choriomeningitis ; Lymphocytic choriomeningitis virus ; Memory T Cells ; Signal Transduction
Chemical Substances	Hepatitis A Virus Cellular Receptor 2 ; Havcr2 protein, mouse
Language	English
Publishing date	2023-12-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2300401
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Article ; Online: Control of T lymphocyte fate decisions by PI3K signaling.

Murter, Benjamin / Kane, Lawrence P

F1000Research

2020 Volume 9

Abstract: Virtually all aspects of T and B lymphocyte development, homeostasis, activation, and effector function are impacted by the interaction of their clonally distributed antigen receptors with antigens encountered in their respective environments. Antigen ... ...

Abstract	Virtually all aspects of T and B lymphocyte development, homeostasis, activation, and effector function are impacted by the interaction of their clonally distributed antigen receptors with antigens encountered in their respective environments. Antigen receptors mediate their effects by modulating intracellular signaling pathways that ultimately impinge on the cytoskeleton, bioenergetic pathways, transcription, and translation. Although these signaling pathways are rather well described at this point, especially those steps that are most receptor-proximal, how such pathways contribute to more quantitative aspects of lymphocyte function is still being elucidated. One of the signaling pathways that appears to be involved in this "tuning" process is controlled by the lipid kinase PI3K. Here we review recent key findings regarding both the triggering/enhancement of PI3K signals (via BCAP and ICOS) as well as their regulation (via PIK3IP1 and PHLPP) and how these signals integrate and determine cellular processes. Lymphocytes display tremendous functional plasticity, adjusting their metabolism and gene expression programs to specific conditions depending on their tissue of residence and the nature of the infectious threat to which they are responding. We give an overview of recent findings that have contributed to this model, with a focus on T cells, including what has been learned from patients with gain-of-function mutations in PI3K as well as lessons from cancer immunotherapy approaches.
MeSH term(s)	Cell Differentiation ; Humans ; Phosphatidylinositol 3-Kinases/metabolism ; Signal Transduction ; T-Lymphocytes/cytology ; T-Lymphocytes/enzymology
Language	English
Publishing date	2020-09-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2699932-8
ISSN	2046-1402 ; 2046-1402
ISSN (online)	2046-1402
ISSN	2046-1402
DOI	10.12688/f1000research.26928.1
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Article ; Online: Control of T lymphocyte fate decisions by PI3K signaling [version 1; peer review

Benjamin Murter / Lawrence P. Kane

F1000Research, Vol

2 approved]

2020 Volume 9

Abstract	Virtually all aspects of T and B lymphocyte development, homeostasis, activation, and effector function are impacted by the interaction of their clonally distributed antigen receptors with antigens encountered in their respective environments. Antigen receptors mediate their effects by modulating intracellular signaling pathways that ultimately impinge on the cytoskeleton, bioenergetic pathways, transcription, and translation. Although these signaling pathways are rather well described at this point, especially those steps that are most receptor-proximal, how such pathways contribute to more quantitative aspects of lymphocyte function is still being elucidated. One of the signaling pathways that appears to be involved in this “tuning” process is controlled by the lipid kinase PI3K. Here we review recent key findings regarding both the triggering/enhancement of PI3K signals (via BCAP and ICOS) as well as their regulation (via PIK3IP1 and PHLPP) and how these signals integrate and determine cellular processes. Lymphocytes display tremendous functional plasticity, adjusting their metabolism and gene expression programs to specific conditions depending on their tissue of residence and the nature of the infectious threat to which they are responding. We give an overview of recent findings that have contributed to this model, with a focus on T cells, including what has been learned from patients with gain-of-function mutations in PI3K as well as lessons from cancer immunotherapy approaches.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	F1000 Research Ltd
Document type	Article ; Online
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Article ; Online: Complementary HLH susceptibility factors converge on CD8 T-cell hyperactivation.

Landy, Emily / Varghese, Jemy / Dang, Vinh / Szymczak-Workman, Andrea / Kane, Lawrence P / Canna, Scott W

Blood advances

2023 Volume 7, Issue 22, Page(s) 6949–6963

Abstract: Hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS) are life-threatening hyperinflammatory syndromes. Familial HLH is caused by genetic impairment of granule-mediated cytotoxicity (eg, perforin deficiency). MAS is linked to ... ...

Abstract	Hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS) are life-threatening hyperinflammatory syndromes. Familial HLH is caused by genetic impairment of granule-mediated cytotoxicity (eg, perforin deficiency). MAS is linked to excess activity of the inflammasome-activated cytokine interleukin-18 (IL-18). Though individually tolerated, mice with dual susceptibility (Prf1⁻/⁻Il18tg; DS) succumb to spontaneous, lethal hyperinflammation. We hypothesized that understanding how these susceptibility factors synergize would uncover key pathomechanisms in the activation, function, and persistence of hyperactivated CD8 T cells. In IL-18 transgenic (Il18tg) mice, IL-18 effects on CD8 T cells drove MAS after a viral (lymphocytic choriomeningitis virus), but not innate (toll like receptor 9), trigger. In vitro, CD8 T cells also required T-cell receptor (TCR) stimulation to fully respond to IL-18. IL-18 induced but perforin deficiency impaired immunoregulatory restimulation-induced cell death (RICD). Paralleling hyperinflammation, DS mice displayed massive postthymic oligoclonal CD8 T-cell hyperactivation in their spleens, livers, and bone marrow as early as 3 weeks. These cells increased proliferation and interferon gamma production, which contrasted with increased expression of receptors and transcription factors associated with exhaustion. Broad-spectrum antibiotics and antiretrovirals failed to ameliorate the disease. Attempting to genetically "fix" TCR antigen-specificity instead demonstrated the persistence of spontaneous HLH and hyperactivation, chiefly on T cells that had evaded TCR fixation. Thus, drivers of HLH may preferentially act on CD8 T cells: IL-18 amplifies activation and demand for RICD, whereas perforin supplies critical immunoregulation. Together, these factors promote a terminal CD8 T-cell activation state, combining features of exhaustion and effector function. Therefore, susceptibility to hyperinflammation may converge on a unique, unrelenting, and antigen-dependent state of CD8 T-cell hyperactivation.
MeSH term(s)	Mice ; Animals ; Lymphohistiocytosis, Hemophagocytic/etiology ; Perforin/genetics ; Perforin/metabolism ; Interleukin-18/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; Receptors, Antigen, T-Cell/metabolism
Chemical Substances	Perforin (126465-35-8) ; Interleukin-18 ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2023-09-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023010502
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Article ; Online: Antigen receptor kinase two-step.

Kane, Lawrence P

Journal of immunology (Baltimore, Md. : 1950)

2014 Volume 193, Issue 9, Page(s) 4277–4278

MeSH term(s)	Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/metabolism
Chemical Substances	Receptors, Antigen, T-Cell ; Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2014-11-01
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1402287
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Article: Immune regulation by Tim-3.

Banerjee, Hridesh / Kane, Lawrence P

F1000Research

2018 Volume 7, Page(s) 316

Abstract: T-cell immunoglobulin and mucin domain 3 (Tim-3) is a transmembrane protein that in both mice and humans has been shown to possess various functions in a context-dependent manner. Thus, Tim-3 has been associated with both inhibitory and co-stimulatory ... ...

Abstract	T-cell immunoglobulin and mucin domain 3 (Tim-3) is a transmembrane protein that in both mice and humans has been shown to possess various functions in a context-dependent manner. Thus, Tim-3 has been associated with both inhibitory and co-stimulatory function, depending in part on the specific cell type and immune response course. Though originally described on T cells, Tim-3 is now known to be expressed by both lymphoid and non-lymphoid cells within the immune system and even by non-immune cells. In addition, though widely thought of as a negative regulator of immunity, Tim-3 has been shown in more recent studies to have a positive function on both myeloid and lymphoid cells, including T cells. Tim-3 is often expressed at a high level on exhausted T cells in tumors and chronic infection and may engage in crosstalk with other so-called "checkpoint" molecules such as PD-1. Thus, Tim-3 has emerged as a possible therapeutic target, which is being actively explored both pre-clinically and clinically. However, recent research suggests a more complex
Language	English
Publishing date	2018-03-14
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2699932-8
ISSN	2046-1402
ISSN	2046-1402
DOI	10.12688/f1000research.13446.1
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Article ; Online: TIM-3 signaling contributes to the suppressive capacity of Tregs from people with HIV on antiretroviral therapy.

Nieves-Rosado, Hector M / Jacobs, Jana L / Naqvi, Asma / Mellors, John W / Macatangay, Bernard J C / Kane, Lawrence P

Journal of leukocyte biology

2023 Volume 114, Issue 4, Page(s) 368–372

Abstract: TIM-3 expression is increased on peripheral regulatory T cells (Tregs) of virally suppressed persons with HIV-1 on antiretroviral therapy (PWH-ART). However, the relevance of TIM-3 expression in this setting is unclear. We used flow cytometry to evaluate ...

Abstract	TIM-3 expression is increased on peripheral regulatory T cells (Tregs) of virally suppressed persons with HIV-1 on antiretroviral therapy (PWH-ART). However, the relevance of TIM-3 expression in this setting is unclear. We used flow cytometry to evaluate the suppressive phenotype and signaling pathways in peripheral TIM-3- vs TIM-3+ Tregs in PWH-ART. TIM-3+ Tregs showed increased expression of IL-10 compared with persons without HIV-1. In addition, TIM-3+ Tregs displayed elevated signaling and activation, relative to TIM-3- Tregs from the same PWH-ART. Dramatically, TIM-3 blockade restrained the in vitro suppressive capacity of peripheral Tregs. Therefore, our data demonstrate not only that TIM-3 expression by Tregs is associated with an immunosuppressive response among PWH-ART, but also that TIM-3 contributes directly to the enhanced suppressive activity of Tregs in this setting.
MeSH term(s)	Humans ; Hepatitis A Virus Cellular Receptor 2/metabolism ; T-Lymphocytes, Regulatory/metabolism ; HIV Infections/drug therapy ; HIV Infections/metabolism
Chemical Substances	Hepatitis A Virus Cellular Receptor 2
Language	English
Publishing date	2023-06-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1093/jleuko/qiad068
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Article: Mast cell activation is enhanced by Tim1:Tim4 interaction but not by Tim-1 antibodies.

Phong, Binh / Kane, Lawrence P

F1000Research

2016 Volume 5, Page(s) 251

Abstract: Polymorphisms in ... ...

Abstract	Polymorphisms in the
Language	English
Publishing date	2016-03-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2699932-8
ISSN	2046-1402
ISSN	2046-1402
DOI	10.12688/f1000research.8132.2
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Article ; Online: Immune regulation by Tim-3 [version 1; referees

Hridesh Banerjee / Lawrence P. Kane

F1000Research, Vol

2 approved]

2018 Volume 7

Abstract	T-cell immunoglobulin and mucin domain 3 (Tim-3) is a transmembrane protein that in both mice and humans has been shown to possess various functions in a context-dependent manner. Thus, Tim-3 has been associated with both inhibitory and co-stimulatory function, depending in part on the specific cell type and immune response course. Though originally described on T cells, Tim-3 is now known to be expressed by both lymphoid and non-lymphoid cells within the immune system and even by non-immune cells. In addition, though widely thought of as a negative regulator of immunity, Tim-3 has been shown in more recent studies to have a positive function on both myeloid and lymphoid cells, including T cells. Tim-3 is often expressed at a high level on exhausted T cells in tumors and chronic infection and may engage in crosstalk with other so-called “checkpoint” molecules such as PD-1. Thus, Tim-3 has emerged as a possible therapeutic target, which is being actively explored both pre-clinically and clinically. However, recent research suggests a more complex in vivo role for this protein, compared with other targets in this area.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2018-03-01T00:00:00Z
Publisher	F1000 Research Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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