What is class I MHC molecule?
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The structural interaction between the human T-cell receptor (TCR), and the antigenic peptide as linked to a major histocompatibility complex (MHC) molecule are fundamental to the workings of the immune system. Previous work has shown that when a virus or bacteria invades the body, the immune system first breaks up cells infected by the invaders. These infected cells are 'flagged" with a combination of the foreign protein and an MHC molecule and bound to a TCR. Roving T-cells then recognize and destroy these flagged cells. \n\nBut until now, no one has known what the atomic structure of this immune interaction looked like. Harvard researchers, led by Don C. Wiley of the Department of Molecular and Cellular Biology, determined that TCR structure resembles that of another key component of the immune system, antibodies, particularly, the anitgen-binding region. This discovery led the way to the identification of the entire structure of the MHC-TCR complex. \n\nThe research indicates that the antigenic peptide produced by degradation of the invading virus within the cell is held within the MHC binding cleft almost like a hot-dog is held in a bun. This peptide and most of the MHC molecule are engulfed by the TCR. \n\nIn a related study, researchers at the University of Maryland Biotechnology Institute gained new insight into the phenomenon of superantigen creation. In some cases, the TCR-MHC interaction leads to an overreaction by T-cells. This overactive immune creates superantigens have that have been implicated in diseases and complications as varied as toxic shock syndrome, diabetes mellitus and multiple sclerosis. \n\nThe researchers showed for the first time how a superantigen protein (in this case, the peptide toxin produced by the bacterium Staphylococcus aureus) binds to the TCR. The work showed that by bringing the MHC and TCR together directly, regardless of the peptide bound to the MHC, the superantigen circumvents the normal mechanism for T-cell activation by specific peptide-MHC complexes, and triggers a more general reaction instead. \n\nThe basis for the current work can be traced back to 1974, when Drs. Rolf Zinkernagel and Peter Doherty determined that killer T-cells sense infected target cells by the identification of viral antigens displayed on the cell surface in combination with MHC proteins. This process has become known as MHC restriction. The two scientists shared the Nobel prize this year for this work.
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Antigen is any substance that evokes the production of an antibody when introduced into the body. Antigens can enter the body through the respiratory tract, digestive tract, or skin. The most common antigens are proteins such as those found in/on bacteria and viruses.While an antibody Antibody, any of perhaps a million kinds of normally occurring protein molecules that are produced in the body of cells called lymphocytes and that act primarily as a defence against invasion by foreign substances. An important component of the immune system, antibodies are found in the blood of all vertebrates, in the fraction of the blood called gamma globulin.
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Dye-labeled antigens for specific variants of MHC?
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D is a specific response.\n\nSpecificity refers to a specific defense that is activated by a specific antigen and the immune response targets that particular antigen and no others.\n\nNonspecific defenses are the same, regardless of the type of invading agent.  They include physical barriers, phagocytic cells, immunological surveillance, interferons, complement proteins, inflammation, and fever.
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First, the interaction between an APC and a halper T cell is greatly enhanced by the presense of a T cell surface protein called CD4. Present on most helper T cells, CD4 binds to part of the class II MHC proteins. The interactions between CD4 and Class II MHC proteins molecules helps keep the helper T cell and the APC joined while activition of the Th cell occurs. IT is thus activitated by Class II MHC Molecules. Class II MHC are macrophages, B cells and activated T Cells. THese are essentially antibodies. that final part i am not sure. It is true by the transitive property.
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A lymphocyte is a type of white blood cell involved in the human body's immune system.So they produce antibodys.Those produce the proteins.Proteins are polymers built from 20 different L-alpha-amino acids. Proteins are assembled from amino acids using information present in genes. Genes are transcribed into RNA, RNA is then subject to post-transcriptional modification and control, resulting in a mature mRNA that undergoes translation into a protein. mRNA is translated by ribosomes that match the three-base codons of the mRNA to the three-base anti-codons of the appropriate tRNA. The enzyme aminoacyl tRNA synthetase catalyzes the addition of the correct amino acid to their tRNAs.
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Antigens were originally defined as non-self molecules which bound specifically to antibodies. In practice, the term antigen is used to mean any molecule recognized by the immune system. \n\nAntigens which induce adaptive immunity are called immunogens. All immunogens are antigens, and are usually called antigens unless their ability to induce an immune response is being discussed. Some antigens, called haptens, are not immunogenic unless they are covalently linked to immunogenic carriers (usually proteins). Haptens can bind antibodies once the antibodies are produced, but haptens will not induce antibody synthesis on their own. Small non-protein organic molecules, for example the antibiotic penicillin, are haptens.\n\nImmunogenicity is influenced by \n\nthe chemical nature of the antigen. \nthe antigen's size. \nthe antigen's usual presence in the body. \nantigen dose and route and timing of administration. \nwhether the antigen is easily phagocytosed. \nwhether antigen is efficiently presented to T cells on MHC. \nthe maturity of the immune system and specific lymphocytes. \nNote that immunogenicity depends on the immune system as well as on the antigen. \n\nImmunogenicity is generally higher for proteins than for other organic molecules. Protein antigens, which are the predominant sort that activate helper T cells, consequently induce more B cell antibody production, synthesis of IgG or IgA, and generation of memory B and T cells. T-independent antigens, which activate only B cells, induce IgM synthesis but not other adaptive immune responses.\n\nImmunogenicity increases with molecular size and complexity. Haptens are generally non-proteins or they are too small to be immunogenic unless they are covalently attached to a carrier protein molecule. Some carbohydrate antigens can stimulate B cells to secrete IgM in the absence of T cell help but do not elicit IgG or memory cells. Human infants make poor responses to carbohydrate antigens, so early vaccinations with bacterial polysaccharide antigens employ protein carriers. Aggregated proteins are easily phagocytosed and more immunogenic than soluble proteins. Adjuvants, including bacterial products, alum, or oil emulsification of antigen, attract and activate antigen-presenting cells (dendritic cells and macrophages) and slow antigen release to prolong exposure and improve immunogenicity.\n\nEach part of the antigen bound by a unique antibody is called an epitope. Most proteins have several epitopes that are recognized by different B cells and induce a polyclonal antibody response. In a polyclonal response, several clones of B cells each make different antibodies, all able to bind to the same antigen but at different epitopes. Epitopes may be shared by closely related antigens (cross-reactivity), so that antibody made to tetanus toxoid binds tetanus toxin. A protein epitope may be a linear sequence of amino acids or it may be assembled by protein folding. Epitopes with definite three-dimensional shapes and charged amino acids are particularly well recognized by antibodies. External membrane and cell wall molecules, often present in many copies on the pathogen, are common B cell antigens. A small peptide of 4-6 amino acids could fit into an antibody binding site, but larger proteins have more extended epitopes across their surfaces.\n\nActive immunity is induced by exposure to antigen. Antigen dose and the route and timing of antigen contact, as well as immunogenicity, influence the magnitude and nature of the immune response. Very high or very low doses of antigen induce tolerance, the inability to respond to that antigen, while intermediate doses induce immunity. We are generally tolerant to cell-bound and soluble antigens present in our own bodies. Oral tolerance to foods is common, although some foods induce allergic reactions. \n\nAntigens encountered in body tissues through subcutaneous or intramuscular injection are carried by lymph and macrophages into the lymph
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There are two:\nThe universal donor is Type O-\nThe universal receiver is Type AB+
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Generally polyclonal anitbodies are used to bind non-specifically to antigens. For instance, you might use monoclonal antibodies to specifically bind to your protein of intererst. You might then use polyclonal Ab to bind the rest of the proteins i.e. to block off the other available 'slots'
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It is an antibody that recognizes and inhibits vascular epithelial growth factor, or VEGF. It would have the standard structure of an antibody, with a heavy chain and a light chain, and a binding pocket specifically to bind VEGF. I'm sure that the binding region is probably proprietary to Genentech. This is a humanized anitbody, meaning that it was developed in mouse and converted into a human antibody so that it can be used as a therapeutic without causing an allergic response.
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TCATTG\n\nT molecules connect with A molecules\nC molecules connect with G molecules
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The D1 protein, also known as the 32-kDa thylakoid membrane protein, is a key component of the photosynthetic electron transport chain acting at the reducing side of photosystem II.\n\nSee the links below for more information. \n\nHope this helps!
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http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=iga.section.962\nhttp://www.ndsu.edu/ndsu/abergstr/webcourses/genetics/tpt/tpt01.htm\n\nHope this helps!
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the main part of specific immune system is Tcell and Bcell...it's hard to explain in details but i try to sum up,when the antigen enters the bode Tcell works a APC and receives antigene parts by MHC on it,MHC stimulate the Tcell to produce IL and INF and these stimulate Bcells to produce specific antibodies against Ag...some of these antibodies destroy the Ag by stimulating the complements and other parts of immune system and some Bcells convert to memory cells for the next time
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To be immunogenic, a molecule needs to be "large enough" or attached to a large molecule.  The epitopes must be different to those in the body; the "self".\n\nThere are other factors.\n\nThis is a good site on Immunology:\n\nhttp://pathmicro.med.sc.edu/book/immunol-sta.htm
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Here is a very good, highly detailed, lavishly illustrated introduction to immunology (click the word "Immunology" on \nthe left).  Since you are in your third year of med school, you shouldn't have any trouble working your way through this.\n\nhttp://www.cehs.siu.edu/fix/medmicro/index.html
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It is not chemistry.  There is some unknown trigger that causes your body (B cells that have differentiated into plasma cells to be specific)to begin producing antibodies to your own proteins or DNA or RNA, etc.  These antibodies are called autoantibodies.