Making Weak Antigens Strong: Coupling Antigens to Red Blood Cells

2021 ◽  
Vol 2021 (9) ◽  
pp. pdb.prot099986
Author(s):  
Edward A. Greenfield ◽  
James DeCaprio ◽  
Mohan Brahmandam
Keyword(s):  
Red Blood Cells ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Receptor Binding ◽  
Blood Cells ◽  
Cell Receptor ◽  
Coupling Methods ◽  
Chromic Chloride ◽  
Almost All ◽  
Chemical Groups

Coupling antigens to red blood cells (RBCs) can increase the immunogenicity of weak antigens. Their size slows dispersal; that, and their particulate nature, also make them good targets for phagocytosis. If the source of the cells is different from the animal to be injected, they can also provide good targets for MHC class II–T-cell receptor binding. The choice of coupling method will depend on the antigen, but because of the complexity of proteins found on the surface of the RBCs, almost all chemical groups are available for coupling. Commonly used coupling methods include tannic acid, chromic chloride, and glutaraldehyde.

scholarly journals Single MHC Mutation Eliminates Enthalpy Associated with T Cell Receptor Binding

2007 ◽  
Vol 373 (2) ◽  
pp. 315-327 ◽  
Author(s):  
Peter J. Miller ◽  
Yael Pazy ◽  
Brian Conti ◽  
David Riddle ◽  
Ettore Appella ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Receptor Binding ◽  
Cell Receptor

scholarly journals Crystallographic and Mutational Data Show That the Streptococcal Pyrogenic Exotoxin J Can Use a Common Binding Surface for T-cell Receptor Binding and Dimerization

2004 ◽  
Vol 279 (37) ◽  
pp. 38571-38576 ◽  
Author(s):  
Heather M. Baker ◽  
Thomas Proft ◽  
Phillip D. Webb ◽  
Vickery L. Arcus ◽  
John D. Fraser ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Receptor Binding ◽  
Cell Receptor ◽  
Binding Surface

scholarly journals Endothelial Cells Promote Human Immunodeficiency Virus Replication in Nondividing Memory T Cells via Nef-, Vpr-, and T-Cell Receptor-Dependent Activation of NFAT

2005 ◽  
Vol 79 (17) ◽  
pp. 11194-11204 ◽  
Author(s):  
Jaehyuk Choi ◽  
Jason Walker ◽  
Kristina Talbert-Slagle ◽  
Paulette Wright ◽  
Jordan S. Pober ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Endothelial Cells ◽  
Viral Replication ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Memory T Cells ◽  
Cell Receptor ◽  
Hiv Replication ◽  
Immunodeficiency Virus

ABSTRACT Human endothelial cells (ECs) enhance human immunodeficiency virus (HIV) replication within CD4+ memory T cells by 50,000-fold in a Nef-dependent manner. Here, we report that EC-mediated HIV type 1 replication is also dependent on an intact vpr gene. Moreover, we demonstrate that despite a requirement for engaging major histocompatibility complex (MHC) class II molecules and costimulators, EC-stimulated virus-producing cells (p24high T cells) do not proliferate, nor are they arrested in the cell cycle. Rather, they are minimally activated, sometimes expressing CD69 but not CD25, HLA-DR, VLA-1, or effector cytokines. Blocking antibodies to interleukin 2 (IL-2), IL-6, IL-7, or tumor necrosis factor do not inhibit viral replication. Cyclosporine effectively inhibits viral replication, as does disruption of the NFAT binding site in the viral long terminal repeat. Furthermore, in the presence of ECs, suboptimal T-cell receptor (TCR) stimulation with phytohemagglutinin L supports efficient viral replication, and suboptimal stimulation with toxic shock syndrome toxin 1 leads to viral replication selectively in the TCR-stimulated, Vβ2-expressing T cells. Collectively, these data indicate that ECs provide signals that promote Nef- and Vpr-dependent HIV replication in memory T cells that have been minimally activated through their TCRs. Our studies suggest a mechanism for HIV replication in vivo within the reservoir of circulating memory CD4+ T cells that persist despite antiretroviral therapy and further suggest that maintenance of immunological memory by MHC class II-expressing ECs via TCR signaling may contribute to HIV rebound following cessation of antiretroviral therapy.

Malaria

2019 ◽  
Author(s):  
Angelina Jayakumar ◽  
Zahir Osman Eltahir Babiker
Keyword(s):  
Southeast Asia ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Parasitic Infection ◽  
Sub Saharan Africa ◽  
Anopheline Mosquito ◽  
Sub Saharan ◽  
The Uk ◽  
Almost All ◽  
Human Infections

Malaria is a tropical parasitic infection of the red blood cells caused by the protozoal species Plasmodium falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi. It is transmitted through the bite of the female Anopheles mosquito. The average incubation period is twelve to fourteen days. Congenital and blood-borne transmissions can also occur. P. falciparum and P. vivax account for most human infections but almost all deaths are caused by P. falciparum, with children under five years of age bearing the brunt of morbidity and mortality in endemic countries. P. falciparum is dominant in sub-Saharan Africa whereas P. vivax predominates in Southeast Asia and the Western Pacific. P. ovalae and P. malaria are less common and are mainly found in sub-Saharan Africa. P. knowlesi primarily causes malaria in macaques and is geographically restricted to southeast Asia. While taking a blood meal, the female anopheline mosquito injects motile sporozoites into the bloodstream. Within half an hour, the sporozoites invade the hepatocytes and start dividing to form tissue schizonts. In P. vivax and P. ovale, some of the sporozoites that reach the liver develop into hypnozoites and stay dormant within the hepatocytes for months to years after the original infection. The schizonts eventually rupture releasing daughter merozoites into the bloodstream. The merozoites develop within the red blood cells into ring forms, trophozoites, and eventually mature schizont. This part of the life cycle takes twenty-four hours for P. knowlesi; forty-eight hours for P. falciparum, P. vivax, P. ovale; and seventy-two hours for P. malariae. In P. vivax and P. ovale, some of the sporozoites that reach the liver develop into hypnozoites and stay dormant within the hepatocytes for months to years after the original infection. The hallmark of malaria pathogenesis is parasite sequestration in major organs leading to cytoadherence, endothelial injury, coagulopathy, vascular leakage, pro-inflammatory cytokine production, and tissue inflammation. Malaria is the most frequently imported tropical disease in the UK with an annual case load of around 2000. P. falciparum is the predominant imported species, and failure to take chemoprophylaxis is the commonest risk factor.

Vulnerability of allografts to rejection by MHC class II-restricted T-cell receptor transgenic mice1

2003 ◽  
Vol 75 (8) ◽  
pp. 1415-1422 ◽  
Author(s):  
Major K. Lee ◽  
Xiaolun Huang ◽  
Beth P. Jarrett ◽  
Daniel J. Moore ◽  
Niraj M. Desai ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii

scholarly journals MHC class II engagement inhibits CD99-induced apoptosis and up-regulation of T cell receptor and MHC molecules in human thymocytes and T cell line

FEBS Letters ◽  
2003 ◽  
Vol 546 (2-3) ◽  
pp. 379-384 ◽  
Author(s):  
Min Kyung Kim ◽  
Yoon-La Choi ◽  
Min Kyung Kim ◽  
Seok-Hyung Kim ◽  
Eun Young Choi ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
Mhc Molecules ◽  
Induced Apoptosis

scholarly journals Methods for Quantifying T cell Receptor Binding Affinities and Thermodynamics

2009 ◽  
pp. 359-381 ◽  
Author(s):  
Kurt H. Piepenbrink ◽  
Brian E. Gloor ◽  
Kathryn M. Armstrong ◽  
Brian M. Baker
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Receptor Binding ◽  
Cell Receptor ◽  
Binding Affinities

Structural basis for the recognition of mutant self by a tumor-specific, MHC class II–restricted T cell receptor

2007 ◽  
Vol 8 (4) ◽  
pp. 398-408 ◽  
Author(s):  
Lu Deng ◽  
Ries J Langley ◽  
Patrick H Brown ◽  
Gang Xu ◽  
Leslie Teng ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
Structural Basis
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