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Non-engineered IgM (such as is produced in vivo) has the same binding domain on all "arms" of the pentamer. They don't bind to more than one antigen, instead they can bind to multiple copies of the same epitope. Due to steric hindrance, a single IgM molecule generally will not bind at all 10 binding sites.


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yes, T cells and all other nucleated express MHC class 1 molecules. There are two types of MHC molecules, MHC class 1 and 2. All nucleated cells express MHC 1 molecules when infected (including T cells). Cytotoxic T (CD8) cells only recognise MHC 1 molecules. When cells are infected with viruses, they express MHC 1 molecules.This allows cytotoxic T cells ...


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Problems: Where are the anti-antibodies created? In a mouse or in a human? Well, of course, you can't use humans to create antibodies so we are left with mice. So what's wrong with that? Anti-antibodies will be created to the Fc (the constant section of the antibody) region of the antibody because the antibody is foreign and is treated as a foreign ...


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Yes, we should. But Ebola doesn't completely immunosuppress us, or there would be no survivors. Ebola kills by overwhelming the body before enough antibodies are formed to fight it. If you're one of the survivors (as about 40-50% are, more with good care), you'll have antibodies to Ebola in your blood which might help someone else infected with Ebola. If ...


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This is a pretty broad question, but I will try to give an answer: This process will undergo further evolution over time, no question. It has evolved into the current state and there is no reason to assume that this ended. When there are mutations which prove advantageous, they will evolve. This may also involve a faster response time for example, but we ...


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If you are referring to reducing the titer in the immunized animal, you could give the animal a drug that has immunosuppressive properties. Velcade (PS-341) is a drug that effectively reduces plasma cell counts. There are many immunosuppressive drugs available. If you want to reduce the antibodies affinity, you are undertaking a much more delicate process. ...


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There can be many responses. They are important by alloimmunity (so by transfusion, transplantation, etc...), by recognizing pathogens, cancer, virus, etc... By T cell activation, the regulator T cells recognize these antigens as self, and prevent the autoimmune reaction. I guess they were thinking on MHC1 and MHC2. MHC1 shows the inside of the cells, so ...


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There are other histocompatibility antigens on the surface of blood cells, e.g. A, B, Rh, etc... (There are probably a lot more which change less by person to person, so they have lower effect on the outcome of blood transfusion.) These antigens can be recognized by immune cells as self, that's why they don't destroy them. Before complete differentiation ...


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The situation is just as you'd imagine. In an immunocompetant recipient, a host-versus-graft reaction occurs. This is called transplant rejection. Single episodes (acute rejection) are easy to treat and rarely lead to organ failure. Chronic rejection is the leading cause of organ transplant failure. The organ slowly loses its function and symptoms start to ...


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T-cells are selected against self reactivity so those that react to self-MHC are selected against and die by anergy. That's why they try to match the donor and the recipient's MHC molecules, to diminish the immune response.


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As mentioned in the comment, all antibodies have constant regions and variable regions. The variable regions are the binding sites on the ends of the two arms, and the constant regions are the rest of the molecule. When humans are injected with murine antibodies, the immune system recognises and sets up an immune response to them, through generation of HAMA. ...


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It's common for the human immune system to create antibodies against many proteins, even some human proteins. Hemophiliacs who receive regular doses of clotting factor proteins often develop neutralizing antibodies against the clotting factor proteins, even though they are a human protein1. Therefore it's not surprising that antibodies would be developed ...


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All nucleated cell (cells with defined nucleus) are able to present MHC-1 on their surface. Since red blood cells do not have nucleus, they are not able to represent antigins in MHC-1 molecule. Hope that helps check wikipedia for reference


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The presentation of antigens on the cell surface is done by two different molecule complexes: The MHCI and the MHCII complexes. These are coupled to different pathways and are recognized by different T cell populations. The MHCI molecule presents all proteins which are present in the cell on the surface. To do so, peptides coming from the proteasome (where ...


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Viruses can infect any cell: a virus must have a host cell (bacteria, plant or animal) in which to live and make more viruses. Outside of a host cell, viruses cannot function. Source This includes the dendritic cells: Dendritic cells are antigen-presenting cells of the immune system. Their main function is to process antigen material and present ...



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