Absence of the OKT4 epitope on blood T cells and thymus cells in a patient with thymoma, hypogammaglobulinemia, and red blood cell aplasia

1985 ◽  
Vol 76 (3) ◽  
pp. 433-439 ◽  
Author(s):  
A.I. Levinson ◽  
J.A. Hoxie ◽  
M.J. Kornstein ◽  
D. Zembryki ◽  
D.M. Matthews ◽  
...  
Keyword(s):  
T Cells ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Thymus Cells

scholarly journals Anti-tumor effects of RTX-240: an engineered red blood cell expressing 4-1BB ligand and interleukin-15

2021 ◽  
Author(s):  
Shannon L. McArdel ◽  
Anne-Sophie Dugast ◽  
Maegan E. Hoover ◽  
Arjun Bollampalli ◽  
Enping Hong ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Blood Cell ◽  
Nk Cells ◽  
Red Blood Cell ◽  
Safety Profile ◽  
Nk Cell ◽  
Cell Activity ◽  
In Vivo Studies

AbstractRecombinant agonists that activate co-stimulatory and cytokine receptors have shown limited clinical anticancer utility, potentially due to narrow therapeutic windows, the need for coordinated activation of co-stimulatory and cytokine pathways and the failure of agonistic antibodies to recapitulate signaling by endogenous ligands. RTX-240 is a genetically engineered red blood cell expressing 4-1BBL and IL-15/IL-15Rα fusion (IL-15TP). RTX-240 is designed to potently and simultaneously stimulate the 4-1BB and IL-15 pathways, thereby activating and expanding T cells and NK cells, while potentially offering an improved safety profile through restricted biodistribution. We assessed the ability of RTX-240 to expand and activate T cells and NK cells and evaluated the in vivo efficacy, pharmacodynamics and tolerability using murine models. Treatment of PBMCs with RTX-240 induced T cell and NK cell activation and proliferation. In vivo studies using mRBC-240, a mouse surrogate for RTX-240, revealed biodistribution predominantly to the red pulp of the spleen, leading to CD8 + T cell and NK cell expansion. mRBC-240 was efficacious in a B16-F10 melanoma model and led to increased NK cell infiltration into the lungs. mRBC-240 significantly inhibited CT26 tumor growth, in association with an increase in tumor-infiltrating proliferating and cytotoxic CD8 + T cells. mRBC-240 was tolerated and showed no evidence of hepatic injury at the highest feasible dose, compared with a 4-1BB agonistic antibody. RTX-240 promotes T cell and NK cell activity in preclinical models and shows efficacy and an improved safety profile. Based on these data, RTX-240 is now being evaluated in a clinical trial.

scholarly journals Control of Plasmodium falciparum erythrocytic cycle: γδ T cells target the red blood cell–invasive merozoites

Blood ◽  
2011 ◽  
Vol 118 (26) ◽  
pp. 6952-6962 ◽  
Author(s):  
Giulia Costa ◽  
Séverine Loizon ◽  
Marianne Guenot ◽  
Iulia Mocan ◽  
Franck Halary ◽  
...  
Keyword(s):  
T Cells ◽  
Plasmodium Falciparum ◽  
T Cell ◽  
Blood Cell ◽  
Parasite Density ◽  
Red Blood Cell ◽  
Γδ T Cells ◽  
Γδ T Cell ◽  
Antiparasitic Activity ◽  
Vγ9vδ2 T Cells

AbstractThe control of Plasmodium falciparum erythrocytic parasite density is essential for protection against malaria, because it prevents pathogenesis and progression toward severe disease. P falciparum blood-stage parasite cultures are inhibited by human Vγ9Vδ2 γδ T cells, but the underlying mechanism remains poorly understood. Here, we show that both intraerythrocytic parasites and the extracellular red blood cell–invasive merozoites specifically activate Vγ9Vδ2 T cells in a γδ T cell receptor–dependent manner and trigger their degranulation. In contrast, the γδ T cell–mediated antiparasitic activity only targets the extracellular merozoites. Using perforin-deficient and granulysin-silenced T-cell lines, we demonstrate that granulysin is essential for the in vitro antiplasmodial process, whereas perforin is dispensable. Patients infected with P falciparum exhibited elevated granulysin plasma levels associated with high levels of granulysin-expressing Vδ2+ T cells endowed with parasite-specific degranulation capacity. This indicates in vivo activation of Vγ9Vδ2 T cells along with granulysin triggering and discharge during primary acute falciparum malaria. Altogether, this work identifies Vγ9Vδ2 T cells as unconventional immune effectors targeting the red blood cell–invasive extracellular P falciparum merozoites and opens novel perspectives for immune interventions harnessing the antiparasitic activity of Vγ9Vδ2 T cells to control parasite density in malaria patients.

scholarly journals Hybrid red blood cell membrane coated porous silicon nanoparticles functionalized with cancer antigen induce depletion of T cells

RSC Advances ◽  
2020 ◽  
Vol 10 (58) ◽  
pp. 35198-35205
Author(s):  
Antti Rahikkala ◽  
Flavia Fontana ◽  
Tomás Bauleth-Ramos ◽  
Alexandra Correia ◽  
Marianna Kemell ◽  
...  
Keyword(s):  
T Cells ◽  
Porous Silicon ◽  
Cell Membrane ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Peripheral Blood ◽  
Silicon Nanoparticles ◽  
Functionalized Nanoparticles ◽  
Cancer Antigen ◽  
Red Blood Cell Membrane

We report a study on the effect of red blood cell membrane based cancer antigen-functionalized nanoparticles on peripheral blood T cells. These nanoparticles induce apoptosis of T cells and they may have use in treating autoimmune diseases.

scholarly journals Regulatory T-cell status in red cell alloimmunized responder and nonresponder mice

Blood ◽  
2009 ◽  
Vol 113 (22) ◽  
pp. 5624-5627 ◽  
Author(s):  
Weili Bao ◽  
Jin Yu ◽  
Susanne Heck ◽  
Karina Yazdanbakhsh
Keyword(s):  
T Cells ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Major Complication ◽  
Glycophorin A ◽  
Red Cell ◽  
Suppressive Activity ◽  
Human Glycophorin

Abstract Red blood cell alloimmunization remains a major complication for transfusion-dependent patients, but immune factors governing risk for alloimmunization are unknown. We hypothesized that CD4+ regulatory T cells (Tregs), which we have shown control the rate and the frequency of red blood cell alloimmunization in mouse models, may dictate responder/nonresponder status. Using a transfusion regimen in which more than 50% of mice develop alloantibodies to human glycophorin A antigen, we found reduced in vitro and in vivo Treg-suppressive activity in responders compared with nonresponders that was the result of impaired Treg suppressor function. Moreover, responders were prone to developing additional alloantibodies to strong immunogens, whereas nonresponders were resistant to alloimmunization. Altogether, our data raise the possibility that Treg activity may be used as a marker for identifying responder/nonresponder status in transfusion recipients.

scholarly journals Stored Red Blood Cell Transfusion Induces Regulatory T Cells

2009 ◽  
Vol 208 (1) ◽  
pp. 110-119 ◽  
Author(s):  
Joel M. Baumgartner ◽  
Christopher C. Silliman ◽  
Ernest E. Moore ◽  
Anirban Banerjee ◽  
Martin D. McCarter
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Red Blood Cell Transfusion

scholarly journals Phenotypic differences of CD4+T cells in response to red blood cell immunization in transfused sickle cell disease patients

2015 ◽  
Vol 45 (6) ◽  
pp. 1868-1879 ◽  
Author(s):  
Benoît Vingert ◽  
Marie Tamagne ◽  
Anoosha Habibi ◽  
Sadaf Pakdaman ◽  
Julie Ripa ◽  
...  
Keyword(s):  
T Cells ◽  
Sickle Cell Disease ◽  
Blood Cell ◽  
Sickle Cell ◽  
Red Blood Cell ◽  
Cd4 T Cells ◽  
Cell Disease ◽  
Phenotypic Differences

scholarly journals Clonal regulatory T cells specific for a red blood cell autoantigen in human autoimmune hemolytic anemia

Blood ◽  
2008 ◽  
Vol 111 (2) ◽  
pp. 680-687 ◽  
Author(s):  
Frank J. Ward ◽  
Andrew M. Hall ◽  
Lindsay S. Cairns ◽  
Arabella S. Leggat ◽  
Stanislaw J. Urbaniak ◽  
...  
Keyword(s):  
T Cells ◽  
Blood Cell ◽  
Hemolytic Anemia ◽  
Red Blood Cell ◽  
Autoimmune Hemolytic Anemia ◽  
Ex Vivo ◽  
Interleukin 10 ◽  
Regulatory Function ◽  
Antigen Specificity ◽  
T Helper 1

Regulatory T (Tr) cells have the potential to treat immune-mediated disease, but cloning such cells for study from patients with autoimmune disease has proven difficult. Here, we describe autoantigen-specific, interleukin-10 (IL-10)–secreting Tr cell clones recovered ex vivo from a patient with autoimmune hemolytic anemia (AIHA) and characterize their phenotype, origin, and regulatory function. These IL-10+ Tr cells recognized a peptide, 72H-86L, derived from the Rh red blood cell autoantigen and shared phenotypic characteristics with both natural and inducible Tr cells. The clones also expressed different Tr markers depending on activation state: high levels of CD25 and LAG-3 when expanding nonspecifically, but FoxP3 after activation by the autoantigen they recognize. Despite a discrete Tr phenotype, these cells stably expressed the T helper 1 (Th1) signature transcription factor T-bet, suggesting they derive from Th1 T cells. Finally, the contribution of CTLA-4 in activating these IL-10+ Tr cells was confirmed by analyzing responses to transgenic B7.1-like molecules that preferentially bind either CD28 or CTLA-4. Overall, these Tr cells have a functional phenotype different from those described in previous studies of human Tr populations, which have not taken account of antigen specificity, and understanding their properties will enable them to be exploited therapeutically in AIHA.

Red blood cell supernatant induces regulatory t cells independent of leukoreduction or free hemoglobin

2008 ◽  
Vol 207 (3) ◽  
pp. S42
Author(s):  
Joel M. Baumgartne ◽  
Ernest E. Moore ◽  
Anirban Banerjee ◽  
Christopher Silliman ◽  
Martin McCarter
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Free Hemoglobin ◽  
Cell Supernatant
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