Induction of immunologic tolerance to thymus-dependent antigen (sheep's red blood cells) in the absence of T cells

1979 ◽  
Vol 87 (1) ◽  
pp. 31-34
Author(s):  
T. K. Novikova ◽  
I. A. Kondrat'eva ◽  
L. N. Fontalin
Keyword(s):  
T Cells ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Immunologic Tolerance ◽  
Sheep's Red Blood Cells

Effect of immune complexes on electrophoretic mobility of sheep's red blood cells

1990 ◽  
Vol 109 (3) ◽  
pp. 365-367
Author(s):  
N. A. Konstantinova ◽  
A. M. Sapozhnikov
Keyword(s):  
Red Blood Cells ◽  
Electrophoretic Mobility ◽  
Immune Complexes ◽  
Blood Cells ◽  
Sheep's Red Blood Cells

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.

scholarly journals Freeze-thaw lysates of Plasmodium falciparum-infected red blood cells induce differentiation of functionally competent regulatory T cells from memory T cells

2012 ◽  
Vol 42 (7) ◽  
pp. 1767-1777 ◽  
Author(s):  
Olivia C. Finney ◽  
Emma Lawrence ◽  
Alice P. Gray ◽  
Madi Njie ◽  
Eleanor M. Riley ◽  
...  
Keyword(s):  
T Cells ◽  
Plasmodium Falciparum ◽  
Regulatory T Cells ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Memory T Cells ◽  
Freeze Thaw

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

Murine T cells reactive against autologous erythrocytes: Evidence for in vitro and in vivo priming with mouse and rat red blood cells

1987 ◽  
Vol 106 (1) ◽  
pp. 53-61 ◽  
Author(s):  
D.C. Hooper ◽  
J.L. Young ◽  
C.J. Elson ◽  
R.B. Taylor
Keyword(s):  
T Cells ◽  
Red Blood Cells ◽  
Blood Cells
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