Immunology: MHC-I expression patterns?
545171
Yes all the 6 HLA 1 alleles are expressed in all nucleated cells because they are codominant.
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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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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation \nORRESPONDENCE Daniel J. Cua: daniel.cua@dnax.org\n\nInterleukin (IL)-23 is a heterodimeric cytokine composed of a unique p19 subunit, and a common p40 subunit shared with IL-12. IL-12 is important for the development of T helper (Th)1 cells that are essential for host defense and tumor suppression. In contrast, IL-23 does not promote the development of interferon-{gamma}–producing Th1 cells, but is one of the essential factors required for the expansion of a pathogenic CD4+ T cell population, which is characterized by the production of IL-17, IL-17F, IL-6, and tumor necrosis factor. Gene expression analysis of IL-23–driven autoreactive T cells identified a unique expression pattern of proinflammatory cytokines and other novel factors, distinguishing them from IL-12–driven T cells. Using passive transfer studies, we confirm that these IL-23–dependent CD4+ T cells are highly pathogenic and essential for the establishment of organ-specific inflammation associated with central nervous system autoimmunity.\n\nAbbreviations used: CIA, collagen-induced arthritis; CNS, central nervous system; DLN, draining LN; EAE, experimental autoimmune encephalomyelitis; MOG, myelin-oligodendrocyte glycoprotein peptide; PLP, proteolipid protein peptide.\n\nClaire L. Langrish1, Yi Chen1, Wendy M. Blumenschein2, Jeanine Mattson2, Beth Basham3, Jonathan D. Sedgwick1, Terrill McClanahan2, Robert A. Kastelein1, and Daniel J. Cua1\n\n1 Discovery Research, DNAX Research Inc., Palo Alto, CA 94304\n2 Experimental Pathology and Pharmacology, DNAX Research Inc., Palo Alto, CA 94304\n3 Bioinformatics, DNAX Research Inc., Palo Alto, CA 94304 \n\nPublished 18 January 2005. doi:10.1084/jem.20041257\n© Rockefeller University Press, 0022-1007 $8.00\nJEM, Volume 201, Number 2, 233-240
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activated lymphocytes (B cells and T cells) during an infection
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self-cells have their own protein marker(protein embedded in the cell surface ) that will differentiate the self-cells with non-self cells.We have our own immune system(white blood cells or T-cells/marcophages/B-cells).This immune system will monitor and differentiate our cells using the antigen(protein embedded in the cell surface).If the cells does not have this kind of self marker,marcophages will activated and stimulate the T-cells to attack the cells(non-cells)
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http://dev.biologists.org/cgi/content/full/130/17/4123?ck=nck
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i\nii\niii\niv\nv\nvi
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Part of the cell mediated antigen-antibody defense system.
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I did a google search and found lots of lab write-ups and discussions of research, but not an easy educational source. \nYou might want to try wikibooks.\nHere's a link to one of the searches I did for you.\nhttp://en.wikibooks.org/wiki/Immunology_-_Experimental_Methods_in_Immunology
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T cells are one of the variety of white blood cells which are part of the immune system. The immune system as a whole learns very early to distinguish between 'self' and 'non-self' sorts of things. The test is largely like this: "is this thing I see something acceptable (ie, self)? If not, kill it." Although the question is posed and answered in a biochemical sort of way. Self is flagged, most fundamentally as near as we can tell, by the presence of Human Leucocyte Antigens (HLA) on the surface of cells. These are highly variable things, so variable that no other person anywhere is more than a tiny bit likely to have the same bunch of them on their cells. Except, of course, for identical twins. \n\nSo T-cells transplanted into you from someone else with fail the 'is this self?' test and will be attacked as 'foreign' by your immune system. They will not survive and will provide very little beneficial effect. It's called the transplant reaction and various aspects of it have earned several Nobel Prizes. \n\nMore speculatively, it may be that immune system tissues have learned to work together, and that, in each person, the exact details of just how to do so may vary. So how my T-cells work might be just enough different than yours that, even if they could survive inside you, they might not be able to interact with the rest of your immune system so as to help much. For instance, one of the things T-cells do is to talk to other immune system cells and direct their operations; if your immune system won't listen to my T-cells, much of what they'd be trying to do would be futile.  \n\nThere is quite a bit more to learn about the detailed workings of the immune system.\n\nBlood type differences (Types A, B, O are the major gropus, but there are many subgroups such as Rh (+/-), S, ...) are a simpler version of this self / non-self business, this time involving rather fewer genes and markers on blood cells. Nevertheless, there are some antibodies (yet another immune system mechanism) which use them to recognize self v non-self, and a transfusion of the wrong blood type will cause a very severe reaction, so severe as to be life-threatening.
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Abstract. \n...membranes, microvilli, and membrane projections, and act as crosslinkers between the actin cytoskeleton and proteins of the cell surface...\nhttp://147.52.72.117/IJO/2002/volume21/number5/935-940.pdf \n\n \nforthcoming meetings\nAim: to learn techniques commonly used to analyse signal transduction ... and cell adhesion (cytoskeleton, cell adhesion proteins, extracellular\nhttp://www.usgeb.ch/skmb2005.html \n\n \nBTO\n...and function of proteins, methods of ... Cytoskeleton and cell motility. ... Describe and use structure determination techniques to analyse\nhttp://www.bto.ed.ac.uk/courses/year1/index0506.phtml \n\n \nRandall Division o f Cell and Molecular Biophysics\n...actin cytoskeleton during migration. I use a number of different advanced imaging techniques to analyse ... analysis of interacting proteins by\nhttp://www.kcl.ac.uk/depsta/biomedical/randall/mparsons.html \n\n \nGlossaire (ULg)\nAnkyrins. A family of membrane-associated proteins responsible for the attachment of the cytoskeleton. Note: membrane proteins \nhttp://www.ebm.lib.ulg.ac.be/prostate/gloss.htm \n\n \nThe role of the axolemma in the initiation of traumatically induced...\n...proteins. Transmembrane proteins such ... matrix to the cytoskeleton via the ... Biophysical investigations have used novel techniques to\nhttp://www.jnnp.com/cgi/content/full/64/3/285 \n\n \nThe tiniest parts of \n...are as dispart as the techniques and ... natural science, is to analyse the ... energy or information, signal transducers, cytoskeleton...\nhttp://www.uni-leipzig.de/~philos/psarros/preprints/the_tiniest_parts_of.html \n\n \nGenome Biology | Full text | Analysis and functional classification\n...as well as the development of new techniques for ... genes encoding cytoskeleton proteins (such as myosin, actin, UNC-87, troponin T) and\nhttp://genomebiology.com/2003/4/4/R26 \n\n \nStudy Abroad 2004 INTRODUCTION 2 Deakin University's unique Study \nUnit Handbook GUIDE TO UNIT DESCRIPTIONS ACD206/306 Dance Production and Analysis Second semester, 1 credit point Prerequisite ACD203 or Level One \nhttp://www.deakin.edu.au/international/Documents/Brochures/SAHandbook.pdf \n\n \nAdrian Harwood\n...genetic, biochemical and cell biological techniques to analyse the ... has both a cytoskeleton and a network ... SH2 domain proteins,\nhttp://www.ucl.ac.uk/LMCB/pages/harwood.html
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It sort of depends on the invader...\n\nFor inanimate stuff--splinters of wood, glass, metal or whatever--the first thing that happens is that there is damage to cells.  Numerous compounds are released, including (but not restricted to) arachnidonic acid.  Now arachnidonic acid is converted into any one of a number of prostaglandins and leukotrienes, becoming a chemical signal that triggers a cascade of responses, including the initiation of inflammation and the attraction of an assortment of cells, including fibroblasts, macrophages and other leukocytes, and a few other critters.  Sometimes, there is enough pus formed by degenerating leukocytes that the foreign body is induced to extrude.  Other times, there is formation of a fibrous capsule around the foreign body, encapsulating it and walling it away from everything else.\n\nNow, looking at an "animate" invader, let's take the case of a bacterium...  Leukocytes are attracted to the area by substances produced locally.  Some, such as polymorphonuclear neutrophils, will actually engulf the bacteria and digest them, or at least try to (Some are too tough; mycobacteria are among 'em); macrophages will do that too.  Now, one group of leukocytes, and as I recall it that's the macrophages, will identify sections on the outside of the bacteria that look like good things to build antibodies against, and will "present" those things to lympohcytes, which will be triggered to generate antibodies against them.  As it turns out, the lymphocytes have been preprogrammed to recognize a specific appearance of object (the molecular goings on there are rather complex, but fascinating), and have just been waiting for the chance.  Antibodies will start forming; usually, the first ones will be IgM, a pentavalent antibody: it's sort of like 5 standard antibodies welded into a really big antibody.  Now, with invasion of a mucosal surface (like the lining of the nose or mouth), there is often the divalent IgA produced instead.  Either way, as the response matures, there is generation of a much more specific IgG clone--and it's the IgG antibody (monovalent, but it's Y shaped, more or less, and has two binding sites, at the ends of the arms of the Y) that is the "long term memory" antibody, for the most part.  (Where and how IgD and IgE fit into this, we're still trying to figure, although we've learned that IgE is the antibody of allergy, mainly, but also the one raised against multicellular critters, like Trichinella.)\n\nSimultaneously, of course, the cellular response is running, and as the antibody response is developing there is also the activation of the C-proteins.  That's a whole long story, but these proteins produce a cascade of response that generates an enzyme that rips holes in the outside of the bacteria's cell membrane or cell wall...\n\nThe big difference, of course, with viruses is that they actually invade cells (although Chlamydia, Chlamydophila, Ureaplasma, Mycoplasma, Rickettsia and others do so to, and are more like bacteria), and it is abnormal compounds on the outside of the infected cell that trigger the immune response.  (Some folks have hypothesized that this is one of the things that causes the association between some viral infections and autoimmune diseases, althoguh that's probably only one thing among many)\n\nMercy, I've rambled too long.  I hope that I've made some semblance of sense!!!
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Although gamma delta T cell receptor-bearing lymphocytes (gamma delta T cells) constitute a significant minority of circulating and tissue-associated T lymphocytes, the mechanism responsible for the activation of these cells is unknown. To address this question, resting gamma delta TCR+, CD3+, CD4-, CD8- cells isolated from the blood of healthy volunteers were cultured with allogeneic dendritic cells (DC) or monocytes, and their proliferative response measured. DC alone induced gamma delta T cells to proliferate, with a peak response on the sixth day of culture. Pretreatment of DC with an anti-HLA-DR mAb, but not anti-HLA class I or anti-CD1 mAbs, inhibited the response of gamma delta T cells. Antibodies to gamma delta T cell receptor, CD2, CD3, or CD11a were also inhibitory, whereas antibodies to alpha beta T cell receptor, CD4, CD5, and CD8 had no effect. Although only 40-60% of freshly isolated gamma delta T cells expressed CD28, mAbs directed against CD28 or its ligand, CD80, were markedly inhibitory. Moreover, removal of CD28+ cells from the gamma delta T cell population nearly abrogated the response to DC. These results demonstrate that resting gamma delta T cells recognize and respond to MHC class II determinants on allogeneic DC in a manner that is highly dependent on the CD28 activation pathway as well as molecules such as CD2 and CD11a that mediate cell-to-cell adhesion.
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a) tlc identifies gene products\nb) Southern blots (capitalized) identify genes based on homology aand hybridization\nc) western blots (not capitalized) identify proteins\nd) no such thing as an eastern blot (not capitalized ?)
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The collection and analysis of tissue samples is a long- established technique in pathology. What is new in "molecular pathology" is the emphasis on assessing gene expression in addition to morphology, and the use of gene expression analysis to validate large numbers of targets. (However, histochemistry and immunohistochemistry have been used, for specific proteins, since before the advent of genomics
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FALSE -there is no single gene for each antibody- not at least in the traditional/classical sense (those intact in the zygote, the first cell of an individual).\n\nThere are much more varieties of antibodies than the number of inherited, intact genes. But every variety of antibody can be traced back to one 'constituted gene' (developed in the adult stage, not inherited as a piece). There are fragments of genes that are present in the zygote but randomly mixed later during development. This mixing happens in various combinations to form different types of genes in different antibody-producing cells (lymphocytes). There is also further variety introduced after the RNA is formed. Hence, each cell (lymphocyte) or its clone produces different antibody in our body.
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The immune system is composed of many interdependent cell types that collectively protect the body from bacterial, parasitic, fungal, viral infections and from the growth of tumor cells. Many of these cell types have specialized functions. The cells of the immune system can engulf bacteria, kill parasites or tumor cells, or kill viral-infected cells. Often, these cells depend on the T helper subset for activation signals in the form of secretions formally known as cytokines, lymphokines, or more specifically interleukins. The purpose of this article is to review the organs, cell types and interactions between cells of the immune system as a commentary on their importance and interdependence on the T helper subset. Such an understanding may help comprehend the root of immune deficiencies, and perceive potential avenues that the immune system can be modulated in the case of specific diseases.