scholarly journals Effect Of Human Natural Killer and γδ T Cells on the Growth of Human Autologous Melanoma Xenografts in SCID Mice

2004 ◽  
Vol 64 (1) ◽  
pp. 378-385 ◽  
Author(s):  
Francesco Lozupone ◽  
Daniela Pende ◽  
Vito Lelio Burgio ◽  
Chiara Castelli ◽  
Massimo Spada ◽  
...  
Keyword(s):  
T Cells ◽  
Natural Killer ◽  
Γδ T Cells ◽  
Scid Mice

Blockade of NKG2D signaling prevents the development of murine CD4+ T cell-mediated colitis

2008 ◽  
Vol 294 (1) ◽  
pp. G199-G207 ◽  
Author(s):  
Y. Ito ◽  
T. Kanai ◽  
T. Totsuka ◽  
R. Okamoto ◽  
K. Tsuchiya ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Natural Killer ◽  
Lamina Propria ◽  
Intestinal Inflammation ◽  
Constitutive Expression ◽  
Γδ T Cells ◽  
Scid Mice ◽  
Costimulatory Receptor ◽  
Bowel Diseases

It has been recently demonstrated that NKG2D is an activating costimulatory receptor on natural killer (NK) cells, natural killer T (NKT) cells, activated CD8+ T cells, and γδ T cells, which respond to cellular stress, such as inflammation, transformation, and infection. Here we show that intestinal inflammation in colitic SCID mice induced by adoptive transfer of CD4+CD45RBhigh T cells is characterized by significant increase of CD4+NKG2D+ T cells and constitutive expression of NKG2D ligands, such as H60, Mult-1, and Rae-1, by lamina propria CD11c+ dendritic cells. Furthermore, treatment with nondepleting and neutralizing anti-NKG2D MAb after transfer of CD4+CD45RBhigh T cells into SCID mice significantly suppressed wasting disease with colitis, abrogated leukocyte infiltration, and reduced production of IFN-γ by lamina propria CD4+ T cells. These findings demonstrate that NKG2D signaling pathway is critically involved in CD4+ T cell-mediated disease progression and suggest a new therapeutic target for inflammatory bowel diseases.

scholarly journals Next-generation cell therapies: the emerging role of CAR-NK cells

Hematology ◽  
2020 ◽  
Vol 2020 (1) ◽  
pp. 570-578
Author(s):  
Rafet Basar ◽  
May Daher ◽  
Katayoun Rezvani
Keyword(s):  
T Cells ◽  
Cell Therapy ◽  
Natural Killer ◽  
Γδ T Cells ◽  
Antigen Receptors ◽  
T Cell Therapy ◽  
Cell Therapies ◽  
Immune Effector ◽  
Effector Cells ◽  
Immune Effector Cells

Abstract T cells engineered with chimeric antigen receptors (CARs) have revolutionized the field of cell therapy and changed the paradigm of treatment for many patients with relapsed or refractory B-cell malignancies. Despite this progress, there are limitations to CAR-T cell therapy in both the autologous and allogeneic settings, including practical, logistical, and toxicity issues. Given these concerns, there is a rapidly growing interest in natural killer cells as alternative vehicles for CAR engineering, given their unique biological features and their established safety profile in the allogeneic setting. Other immune effector cells, such as invariant natural killer T cells, γδ T cells, and macrophages, are attracting interest as well and eventually may be added to the repertoire of engineered cell therapies against cancer. The pace of these developments will undoubtedly benefit from multiple innovative technologies, such as the CRISPR-Cas gene editing system, which offers great potential to enhance the natural ability of immune effector cells to eliminate refractory cancers.

scholarly journals Mycobacterium tuberculosis-Specific T Cell Functional, Memory, and Activation Profiles in QuantiFERON-Reverters Are Consistent With Controlled Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Cheleka A. M. Mpande ◽  
Pia Steigler ◽  
Tessa Lloyd ◽  
Virginie Rozot ◽  
Boitumelo Mosito ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Natural Killer ◽  
Mononuclear Cells ◽  
Γδ T Cells ◽  
T Cell Responses ◽  
Th1 Cells ◽  
Functional Responses ◽  
Cell Responses

Reversion of immune sensitization tests for Mycobacterium tuberculosis (M.tb) infection, such as interferon-gamma release assays or tuberculin skin test, has been reported in multiple studies. We hypothesized that QuantiFERON-TB Gold (QFT) reversion is associated with a decline of M.tb-specific functional T cell responses, and a distinct pattern of T cell and innate responses compared to persistent QFT+ and QFT- individuals. We compared groups of healthy adolescents (n=~30 each), defined by four, 6-monthly QFT tests: reverters (QFT+/+/-/-), non-converters (QFT-/-/-/-) and persistent positives (QFT+/+/+/+). We stimulated peripheral blood mononuclear cells with M.tb antigens (M.tb lysate; CFP-10/ESAT-6 and EspC/EspF/Rv2348 peptide pools) and measured M.tb-specific adaptive T cell memory, activation, and functional profiles; as well as functional innate (monocytes, natural killer cells), donor-unrestricted T cells (DURT: γδ T cells, mucosal-associated invariant T and natural killer T-like cells) and B cells by flow cytometry. Projection to latent space discriminant analysis was applied to determine features that best distinguished between QFT reverters, non-converters and persistent positives. No longitudinal changes in immune responses to M.tb were observed upon QFT reversion. M.tb-specific Th1 responses detected in reverters were of intermediate magnitude, higher than responses in QFT non-converters and lower than responses in persistent positives. About one third of reverters had a robust response to CFP-10/ESAT-6. Among those with measurable responses, lower proportions of TSCM (CD45RA+CCR7+CD27+) and early differentiated (CD45RA-) IFN-γ-TNF+IL-2- M.tb lysate-specific CD4+ cells were observed in reverters compared with non-converters. Conversely, higher proportions of early differentiated and lower proportions of effector (CD45RA-CCR7-) CFP10/ESAT6-specific Th1 cells were observed in reverters compared to persistent-positives. No differences in M.tb-specific innate, DURT or B cell functional responses were observed between the groups. Statistical modelling misclassified the majority of reverters as non-converters more frequently than they were correctly classified as reverters or misclassified as persistent positives. These findings suggest that QFT reversion occurs in a heterogeneous group of individuals with low M.tb-specific T cell responses. In some individuals QFT reversion may result from assay variability, while in others the magnitude and differentiation status of M.tb-specific Th1 cells are consistent with well-controlled M.tb infection.

Ex vivo-expanded natural killer cells kill cancer cells more effectively than ex vivo-expanded γδ T cells or αβ T cells

2014 ◽  
Vol 22 (2) ◽  
pp. 486-491 ◽  
Author(s):  
Xuewen Deng ◽  
Hiroshi Terunuma ◽  
Atsushi Terunuma ◽  
Tsubasa Takane ◽  
Mie Nieda
Keyword(s):  
T Cells ◽  
Natural Killer Cells ◽  
Cancer Cells ◽  
Natural Killer ◽  
Ex Vivo ◽  
Γδ T Cells ◽  
Killer Cells ◽  
Αβ T Cells

scholarly journals The cellular immune system in myelomagenesis: NK cells and T cells in the development of MM and their uses in immunotherapies

2015 ◽  
Vol 5 (4) ◽  
pp. e306-e306 ◽  
Author(s):  
T Dosani ◽  
M Carlsten ◽  
I Maric ◽  
O Landgren
Keyword(s):  
T Cells ◽  
Immune System ◽  
Natural Killer ◽  
Γδ T Cells ◽  
Tumor Evolution ◽  
The Status ◽  
And Function ◽  
Cellular Immune ◽  
Functional Profiles ◽  
Killer T Cells

Abstract As vast strides are being made in the management and treatment of multiple myeloma (MM), recent interests are increasingly focusing on understanding the development of the disease. The knowledge that MM develops exclusively from a protracted phase of monoclonal gammopathy of undetermined significance provides an opportunity to study tumor evolution in this process. Although the immune system has been implicated in the development of MM, the scientific literature on the role and status of various immune components in this process is broad and sometimes contradictory. Accordingly, we present a review of cellular immune subsets in myelomagenesis. We summarize the current literature on the quantitative and functional profiles of natural killer cells and T-cells, including conventional T-cells, natural killer T-cells, γδ T-cells and regulatory T-cells, in myelomagenesis. Our goal is to provide an overview of the status and function of these immune cells in both the peripheral blood and the bone marrow during myelomagenesis. This provides a better understanding of the nature of the immune system in tumor evolution, the knowledge of which is especially significant considering that immunotherapies are increasingly being explored in the treatment of both MM and its precursor conditions.

scholarly journals Characterization of Tumor Reactivity of Human Vγ9Vδ2 γδ T Cells In Vitro and in SCID Mice In Vivo

2004 ◽  
Vol 173 (11) ◽  
pp. 6767-6776 ◽  
Author(s):  
Dieter Kabelitz ◽  
Daniela Wesch ◽  
Elke Pitters ◽  
Margot Zöller
Keyword(s):  
T Cells ◽  
Γδ T Cells ◽  
Scid Mice

Flow cytometric analysis of γδ T cells and natural killer cells on HIV-1 infection

1991 ◽  
Vol 58 (1) ◽  
pp. 126-138 ◽  
Author(s):  
Joseph B. Margolick ◽  
Elvia R. Scott ◽  
Nancy Odaka ◽  
Alfered J. Saah
Keyword(s):  
T Cells ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Flow Cytometric Analysis ◽  
Γδ T Cells ◽  
Killer Cells ◽  
Flow Cytometric ◽  
Hiv 1

scholarly journals Cellular Innate Immunity against PRRSV and Swine Influenza Viruses

2019 ◽  
Vol 6 (1) ◽  
pp. 26 ◽  
Author(s):  
Elisa Crisci ◽  
Lorenzo Fraile ◽  
Maria Montoya
Keyword(s):  
Innate Immunity ◽  
T Cells ◽  
Natural Killer ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Γδ T Cells ◽  
Influenza Viruses ◽  
Production Costs ◽  
Respiratory Syndrome Virus

Porcine respiratory disease complex (PRDC) is a polymicrobial syndrome that results from a combination of infectious agents, such as environmental stressors, population size, management strategies, age, and genetics. PRDC results in reduced performance as well as increased mortality rates and production costs in the pig industry worldwide. This review focuses on the interactions of two enveloped RNA viruses—porcine reproductive and respiratory syndrome virus (PRRSV) and swine influenza virus (SwIV)—as major etiological agents that contribute to PRDC within the porcine cellular innate immunity during infection. The innate immune system of the porcine lung includes alveolar and parenchymal/interstitial macrophages, neutrophils (PMN), conventional dendritic cells (DC) and plasmacytoid DC, natural killer cells, and γδ T cells, thus the in vitro and in vivo interactions between those cells and PRRSV and SwIV are reviewed. Likewise, the few studies regarding PRRSV-SwIV co-infection are illustrated together with the different modulation mechanisms that are induced by the two viruses. Alterations in responses by natural killer (NK), PMN, or γδ T cells have not received much attention within the scientific community as their counterpart antigen-presenting cells and there are numerous gaps in the knowledge regarding the role of those cells in both infections. This review will help in paving the way for future directions in PRRSV and SwIV research and enhancing the understanding of the innate mechanisms that are involved during infection with these viruses.

Pediatric CD56+ Anaplastic Large Cell Lymphoma: A Review of the Literature

2006 ◽  
Vol 130 (12) ◽  
pp. 1859-1864
Author(s):  
Cherie H. Dunphy ◽  
Daphne E. DeMello ◽  
Gordon B. Gale
Keyword(s):  
T Cells ◽  
T Cell ◽  
Natural Killer ◽  
Clinical Course ◽  
Γδ T Cells ◽  
Large Cell ◽  
World Health ◽  
Additional Information ◽  
Anaplastic Lymphoma ◽  
Aggressive Clinical Course

Abstract Context.—Anaplastic large cell lymphomas (ALCLs) are a heterogeneous group of CD30+ large cell lymphomas that, according to the World Health Organization classification, are defined as being of T-cell origin, based on immunophenotype, and/or the finding of a T-cell gene rearrangement by molecular studies. Most cases express cytotoxic granule-associated proteins. Relatively recent data have suggested that some T-cell ALCLs are derived from cytolytic CD4+ cells, γδ T cells, or natural killer–like (CD56+ or CD57+) T cells. We encountered a pediatric case of CD56+, anaplastic lymphoma kinase-positive ALCL of apparent natural killer–like T-cell origin (showing positivity for CD2, cytoplasmic CD3, surface CD3 partial positivity, CD7, CD8, CD56, TIA-1, and granzyme B). The patient had initial lymph node and multiple sites of cutaneous involvement and an aggressive clinical course with multiple recurrences after varying periods of complete remission. Objective.—To review the current pediatric literature regarding the incidence, differential diagnosis, and clinical course of such cases. Data Sources.—Relevant articles indexed in PubMed (National Library of Medicine) between 1975 and 2006. Conclusions.—Our review did not confirm a uniformly aggressive clinical course in pediatric cases of CD56+ ALCLs. Such cases suggest the usefulness of the analysis of CD56-positivity in additional cases of ALCL in an attempt to accrue additional information on this condition. Future accrual of such cases may address whether such cases should be treated more aggressively or with possible targeted therapeutic regimens.

Sign in / Sign up

Export Citation Format

Share Document