Surface receptors and immune activity of purified human circulating mononuclear cells. I. The effects of lysis of the sheep red blood cells (SRBC) in the T-cell rosettes on the receptors and cytotoxic activities of the T cells. T cells with receptors for complement

1980 ◽  
Vol 2 (4) ◽  
pp. 349-359 ◽  
Author(s):  
Suzi Sklar ◽  
Margaret Richter ◽  
Gabrielle Ettin ◽  
Maxwell Richter
Keyword(s):  
T Cells ◽  
T Cell ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Mononuclear Cells ◽  
Cytotoxic Activities ◽  
Immune Activity ◽  
Surface Receptors ◽  
Sheep Red Blood Cells

scholarly journals Clonal origin of a T cell lymphoproliferative malignancy

Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 69-76 ◽  
Author(s):  
PA Stryckmans ◽  
L Debusscher ◽  
C Heyder-Bruckner ◽  
R Heimann ◽  
IM Mandelbaum ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Red Blood Cells ◽  
Tumor Cells ◽  
Blood Cells ◽  
Mononuclear Cells ◽  
Polymorphonuclear Cells ◽  
Clonal Origin ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Cell Malignancy

Abstract A woman with a T cell lymphoproliferative malignacy and heterozhgosity at the X chromosome-linked locus for glucose-6-phosphate dehydrogenase (G-6PD) isoenzymes was studied to find the clonal origin of her circulating neoplastic T cells. The red blood cells, polymorphonuclear cells, whole mononuclear cells, and T cell-depleted mononuclear cells contained both A and B isoenzymes of G-6-PD. In contrast, the tumor cells, separated by using their capacity to form rosettes with sheep red blood cells, contained only the B isoenzyme of G-6-PD. This observation strongly suggests the monoclonality of this T cell malignancy.

scholarly journals Clonal origin of a T cell lymphoproliferative malignancy

Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 69-76
Author(s):  
PA Stryckmans ◽  
L Debusscher ◽  
C Heyder-Bruckner ◽  
R Heimann ◽  
IM Mandelbaum ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Red Blood Cells ◽  
Tumor Cells ◽  
Blood Cells ◽  
Mononuclear Cells ◽  
Polymorphonuclear Cells ◽  
Clonal Origin ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Cell Malignancy

A woman with a T cell lymphoproliferative malignacy and heterozhgosity at the X chromosome-linked locus for glucose-6-phosphate dehydrogenase (G-6PD) isoenzymes was studied to find the clonal origin of her circulating neoplastic T cells. The red blood cells, polymorphonuclear cells, whole mononuclear cells, and T cell-depleted mononuclear cells contained both A and B isoenzymes of G-6-PD. In contrast, the tumor cells, separated by using their capacity to form rosettes with sheep red blood cells, contained only the B isoenzyme of G-6-PD. This observation strongly suggests the monoclonality of this T cell malignancy.

scholarly journals Human erythroid burst-promoting activity produced by phytohemagglutinin- stimulated, radioresistant peripheral blood mononuclear cells

Blood ◽  
1979 ◽  
Vol 54 (5) ◽  
pp. 1050-1057 ◽  
Author(s):  
D Meytes ◽  
JA Ma Ortega ◽  
NA Shore ◽  
PP Dukes
Keyword(s):  
T Cell ◽  
Red Blood Cells ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Colony Formation ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Abstract The regulation of erythroid burst-colony formation was studied in cultures of human peripheral blood mononuclear cells. Numbers of erythropoietin-stimulated colonies obtainable from the cells in response to various treatments were compared. One-day preincubation of the cells with phytohemagglutinin (PHA) doubled the yield of colonies. Irradiation of the cells with 3000 rad eliminated their ability to form erythroid bursts, but did not impair the ability of PHA-treated cells to enhance burst formation when added to a fresh batch of cells. This was due to a humoral factor, since media conditioned by PHA-treated washed cells were as effective as the cells themselves. When cells were separated into subpopulations by an adherence procedure and according to their ability to form rosettes with sheep red blood cells, it was found that the PHA-dependent burst-promoting activity released into the medium originated in a nonadherent, nonrosetting (T-cell depleted) cell population.

scholarly journals Inactivated Simian Immunodeficiency Virus-Pulsed Autologous Fresh Blood Cells as an Immunotherapy Strategy

2008 ◽  
Vol 83 (3) ◽  
pp. 1501-1510 ◽  
Author(s):  
Rosemarie D. Mason ◽  
Sheilajen Alcantara ◽  
Viv Peut ◽  
Liyen Loh ◽  
Jeffrey D. Lifson ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Simian Immunodeficiency Virus ◽  
Blood Cells ◽  
Mononuclear Cells ◽  
T Cell Responses ◽  
T Cell Epitopes ◽  
Peripheral Blood Mononuclear ◽  
Cell Responses ◽  
Immunodeficiency Virus

ABSTRACT Practical immunotherapies for human immunodeficiency virus infection are needed. We evaluated inactivated simian immunodeficiency virus (SIV) pulsed onto fresh peripheral blood mononuclear cells in 12 pigtail macaques with chronic SIVmac251 infection for T-cell immunogenicity in a randomized cross-over design study. The immunotherapy was safe and convincingly induced high levels of SIV-specific CD4+ T-cell responses (mean, 5.9% ± 1.3% of all CD4+ T cells) and to a lesser extent SIV-specific CD8+ T-cell responses (mean, 0.7% ± 0.4%). Responses were primarily directed toward Gag and less frequently toward Env but not Pol or regulatory/accessory SIV proteins. T-cell responses against Gag were generally broad and polyfunctional, with a mean of 2.7 CD4+ T-cell epitopes mapped per animal and more than half of the SIV Gag-specific CD4+ T cells expressing three or more effector molecules. The immunogenicity was comparable to that found in previous studies of peptide-pulsed blood cells. Despite the high-level immunogenicity, no reduction in viral load was observed in the chronically viremic macaques. This contrasts with our studies of immunization with peptide-pulsed blood cells during early SIV infection in macaques. Future studies of inactivated virus-pulsed blood cell immunotherapy during early infection of patients receiving antiretroviral therapy are warranted.

NLRP10-Deficient Mice Reveal a Crucial Role for Dendritic Cell Activity in the Initiation of the Allogeneic Response to Transfused Red Blood Cells

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4113-4113
Author(s):  
Stephanie C. Eisenbarth ◽  
Jeanne E Hendrickson ◽  
Samuele Calabro ◽  
Antonia Gallman
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Red Blood Cells ◽  
T Cell Activation ◽  
Blood Cells ◽  
Cell Activation ◽  
Innate Immune ◽  
Deficient Mice

Abstract The generation of antibodies against transfused red blood cells (RBCs) can pose a serious health risk, especially in chronically transfused patients requiring life-long transfusion support; yet our understanding of what immune signals or cells dictate when someone will become alloimmunized is lacking. Every non-autologous red cell unit has multiple antigens foreign to the transfused recipient; some people respond to these foreign antigens with an adaptive immune response and some do not. Given the now well established role of innate immune signals in regulating adaptive immunity, understanding if and how innate immunity is triggered during transfusion may allow development of therapies to prevent alloimmunization in chronically transfused subjects such as those with myelodysplasia or hemoglobinopathies. We have established a murine model system in which we can evaluate both the role of particular innate immune stimuli as well as particular cells of the immune system in regulating the allogeneic response to transfused red blood cells. A particularly useful transgenic “HOD mouse” has been engineered, which encodes a triple fusion protein and provides a unique tool to directly assess both RBC-specific T and B cell responses. This RBC-specific antigen contains the model protein antigen hen egg lysozyme (HEL) fused to chicken ovalbumin (OVA) fused to the human Duffybblood group antigen (HEL-OVA-Duffy) as an integral membrane protein under control of the beta globin promoter. Transfusion of genetically targeted mice lacking various innate immune receptors allows us to screen for important immune pathways regulating the response to allogeneic RBCs. Using these models, we recently discovered that mice lacking the NOD-like receptor NLRP10 fail to develop alloimmunity to transfused red blood cells. Surprisingly, the early innate immune cytokine response, including IL-6, IL-1beta and TNF-alpha, was unaffected in mice lacking NLRP10. Yet both B cell and T cell activation in the spleen to the transgenic transfused RBCs was abrogated. Inclusion of OVA in the alloantigen of the HOD mice allows us to readily study naïve CD4+ T cell activation following transfusion by using the OTII T cell receptor (TCR) transgenic mice in which essentially all T cells express one antigen receptor specific for a peptide of OVA. By tracking rounds of cell division we found that adoptively transferred OTII undergo more than 5-8 rounds of division in the spleen three days following transfusion of HOD RBCs in WT recipients. In contrast, no OTII proliferation was observed in NLRP10-deficient mice following OTII adoptive transfer and HOD RBC transfusion, suggesting that T cells are failing to receive activation signals by splenic antigen presenting cells. We have previously demonstrated that NLRP10-deficient dendritic cells fail to migrate from peripheral tissues such as the skin to draining lymph nodes. Our preliminary data now suggest that NLRP10-deficient dendritic cells are able to process and present RBC-derived antigens, but do not migrate to T cell zones in the spleen to prime naïve RBC-specific T cells. The relative role of dendritic cells, B cells and macrophages in the induction of erythrocyte alloimmunization remain unclear. Further, the need for DC migration within the spleen in the induction of alloimmunity to transfused RBCs has not been addressed. These mice allow us for the first time to answer these fundamental immunologic questions during transfusion. Future work will aim to determine how dendritic cell movement within the spleen is regulated during transfusion in NLRP10-deficient mice and the specific role of splenic dendritic cells in CD4+ T cell priming to allogeneic RBCs. Disclosures No relevant conflicts of interest to declare.

Studies on primed precursors of effector T cells involved in delayed-type hypersensitivity to sheep red blood cells in mice

1987 ◽  
Vol 108 (1) ◽  
pp. 120-131 ◽  
Author(s):  
Shin-ichi Tamura ◽  
Kiyoshi Kikuta ◽  
Toshiaki Kobayashi ◽  
Yuji Sato ◽  
Hiroko Sato
Keyword(s):  
T Cells ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Effector T Cells ◽  
Delayed Type Hypersensitivity ◽  
Sheep Red Blood Cells

scholarly journals Engineered red blood cells as an off-the-shelf allogeneic anti-tumor therapeutic

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Xuqing Zhang ◽  
Mengyao Luo ◽  
Shamael R. Dastagir ◽  
Mellissa Nixon ◽  
Annie Khamhoung ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Checkpoint Inhibitors ◽  
Critical Role ◽  
Cellular Immunotherapy ◽  
Tumor Control

AbstractCheckpoint inhibitors and T-cell therapies have highlighted the critical role of T cells in anti-cancer immunity. However, limitations associated with these treatments drive the need for alternative approaches. Here, we engineer red blood cells into artificial antigen-presenting cells (aAPCs) presenting a peptide bound to the major histocompatibility complex I, the costimulatory ligand 4-1BBL, and interleukin (IL)-12. This leads to robust, antigen-specific T-cell expansion, memory formation, additional immune activation, tumor control, and antigen spreading in tumor models in vivo. The presence of 4-1BBL and IL-12 induces minimal toxicities due to restriction to the vasculature and spleen. The allogeneic aAPC, RTX-321, comprised of human leukocyte antigen-A*02:01 presenting the human papilloma virus (HPV) peptide HPV16 E711-19, 4-1BBL, and IL-12 on the surface, activates HPV-specific T cells and promotes effector function in vitro. Thus, RTX-321 is a potential ‘off-the-shelf’ in vivo cellular immunotherapy for treating HPV + cancers, including cervical and head/neck cancers.

scholarly journals Human erythroid burst-promoting activity produced by phytohemagglutinin- stimulated, radioresistant peripheral blood mononuclear cells

Blood ◽  
1979 ◽  
Vol 54 (5) ◽  
pp. 1050-1057
Author(s):  
D Meytes ◽  
JA Ma Ortega ◽  
NA Shore ◽  
PP Dukes
Keyword(s):  
T Cell ◽  
Red Blood Cells ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Colony Formation ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

The regulation of erythroid burst-colony formation was studied in cultures of human peripheral blood mononuclear cells. Numbers of erythropoietin-stimulated colonies obtainable from the cells in response to various treatments were compared. One-day preincubation of the cells with phytohemagglutinin (PHA) doubled the yield of colonies. Irradiation of the cells with 3000 rad eliminated their ability to form erythroid bursts, but did not impair the ability of PHA-treated cells to enhance burst formation when added to a fresh batch of cells. This was due to a humoral factor, since media conditioned by PHA-treated washed cells were as effective as the cells themselves. When cells were separated into subpopulations by an adherence procedure and according to their ability to form rosettes with sheep red blood cells, it was found that the PHA-dependent burst-promoting activity released into the medium originated in a nonadherent, nonrosetting (T-cell depleted) cell population.

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