i am looking for a way to isolate a subtype of CD4+ Tcells that secrete IL17 using a mo-flo. however i cant stain for IL17 and end up with viable cells. so i figured i could remove all the other effector T cells by staining their cell surface markers with fluorochrome conjugated antibodies and be left with the population i want. but i dont know whether Th1 and Th2 cells have specific cell surface markers.
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Not sure if this will help, but check out this paper:\nhttp://www.nature.com/nature/journal/v415/n6871/full/415536a.html\n\nThis is the abstract:\n\nActivation of naive CD4+ T-helper cells results in the development of at least two distinct effector populations, Th1 and Th2 cells1. Th1 cells produce cytokines (interferon (IFN)-, interleukin (IL)-2, tumour-necrosis factor (TNF)- and lymphotoxin) that are commonly associated with cell-mediated immune responses against intracellular pathogens, delayed-type hypersensitivity reactions4, and induction of organ-specific autoimmune diseases5. Th2 cells produce cytokines (IL-4, IL-10 and IL-13) that are crucial for control of extracellular helminthic infections and promote atopic and allergic diseases4. Although much is known about the functions of these two subsets of T-helper cells, there are few known surface molecules that distinguish between them. We report here the identification and characterization of a transmembrane protein, Tim-3, which contains an immunoglobulin and a mucin-like domain and is expressed on differentiated Th1 cells.
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Apoptosis is characterized by maintenance of intact cell membranes during the suicide process so as to allow adjacent cells to engulf the dying cell so that it does not release its contents and trigger a local inflammatory reaction. Cells undergoing apoptosis usually exhibit a characteristic morphology, including fragmentation of the cell into membrane-bound apoptotic bodies, nuclear and cytoplasmic condensation and endolytic cleavage of the DNA into small oligonucleosomal fragments (Steller, 1995). The cells or fragments are then phagocytosed by macrophages.\n\nSignals that can trigger apoptosis can include\n\nlineage information \ndamage due to ionizing radiation or viral infection \nextracellular signals. \nExtrinsic signals may either suppress or promote apoptosis, and the same signals may promote survival in one cell type and invoke the suicide program in others (Steller, 1995). For example, death receptors that are members of the tumour necrosis factor receptor (TNFR) family sit in cell membranes, but their intracellular domains have direct access to the cell death machinery that lies ready and waiting within the cell (Ashkenazi and Dixit, 1998). When members of the TNF ligand family bind to their receptors some of the pathways activated can include those that bring about cell death. Conversely, there are other factors, such as the neurotrophins, that bind to cell surface receptors and which act to prevent cell death!\n\nInvocation of the suicide program involves the synthesis of specific messenger RNA molecules and their translation. PCD can sometimes be suppressed by inhibiting transcription or translation (Steller, 1995), which provides evidence that cell death is mediated by intrinsic cellular mechanisms.\n\nI'm interested in life! Why do I want to think about death?\nCell death is currently the subject of considerable research activity. This interest stems, in part, from the potential for understanding oncogenesis and the possibility of exploiting the cell death program for therapeutic purposes. For example, inhibition of cell death might contribute to oncogenesis by promoting cell survival instead of death. Likewise, triggering cell death might provide the means for eliminating unwanted cells (e.g., tumor cells).\n\nWhat on Earth has death got to do with development?\nRecognition of PCD as a developmental mechanism dates back well over 100 years (Clark and Clark, 1996; this is an excellent account of old descriptions of "apoptosis" before there was "apoptosis"). Developmental processes that involve PCD include:\n\nElimination of transitory organs and tissues. Examples include phylogenetic vestiges (pronephros and mesonephros in higher vertebrates), anuran tails and gills and larval organs of holometabolous insects. \n\nTissue remodeling. Vertebrate limb bud development (Fig. 11.42, Saunders, 1982; Fig. 1, Saunders, 1966) is an example. If PCD fails, in formation of the digits, digits remain joined by soft tissue. Compare, for example, the situation in the chick and duck hind limbs. If chick limb mesoderm is combined with duck ectoderm, PCD fails and the digits remain joined (Saunders, 1966). This observation implicates the ectoderm in providing the signal to trigger PCD. Another example is formation of heart loops during vertebrate development. Depletion of cells in spinal ganglia occurs during development of the chick embryo. As shown in Table 11.1 (Saunders, 1982), there is precise chronological and spatial control over this process. Interestingly, injections of nerve growth factor reduce the frequency of cell death in the spinal ganglia. This observation provides a link between growth control and PCD.
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You have hives.\n\nFirst, since you have been suffering with urticaria (hives) for over 6 weeks, they are now considered chronic.. One reason the hives are occurring at night is because that is when our cortisol levels are at their lowest, and most chronic hivers find they are worst at night, and some even hive only at night. \n\nAnother problem which causes hiving to worsen at night is that people often have their bodies too warm, and heat is a known mast cell degranulator - mast cells are a special type of immune system cell which contain a bunch of different chemicals, including histamine, which is what causes hives and itching. When mast cells degranulate, they release those chemicals, and being too hot will cause that to happen. Try to sleep in a cool room with minimal covers, that may help.\n\nThird, since you are getting the hives mainly on your chest and back, it is possible the hives are pressure-related. Just the act of lying in bed all night can bring on pressure hives. \n\nHave you tried taking an antihistamine?  For people with chronic urticaria, some antihistamines, such as Ketotifen or Zyrtec, seem to work better than others. And many of us are prescribed off-label dosing, higher than what is used for simple allergies. Plus adding an H2 antihistamine such as Zantac, Tagamet or Pepcid may give you better control of the hives. Some hivers also need a leukotriene blocker (Singulair, Accolate, Zyflo). Others find that adding a mast cell stabilizer (cromolyn, or Ketotifen, which is also an antihistamine) is very helpful. Approx. half of all chronic urticaria sufferers are autoimmune, and for them a course of Cyclosporine can force a remission.\n\nThere is a recipe at the www.chronichives.com website for a lotion you can make using cromolyn which soothes the itchies and calms the rash. And for even more suggestions and information about chronic hives, check out the urticaria support group at yahoo groups - http://health.groups.yahoo.com/group/urt...\n\nYour best bet is to see an allergist/immunologist; they have the most experience in dealing with chronic urticaria. They (usually) know what tests to run, what to rule out, and which meds to use based on what type of chronic urticaria you have.
567140
Consult the proffessionals before you decide.\n\nThe bone marrow produces the white blood corpulses. No other mecinine/tonic helps you grow the WBCs.\n\nA second opinion always helps.\n\nGreat thought, donating. All the best. Take care.
494001
Nope. Exposure is different from active disease. You might want to get a Mantoux (PPD) test. If your rash is larger than a centimeter in the widest diameter, it confirms your exposure (not the disease). Though it also turms positive if you got the BCG vaccine. Active disease is diagnosed by the constellation of signs and symptoms like chronic cough, weight loss, fever, palpable lymph nodes. If you experience any of these, the doctor might request for AFB stain. You submit your sputum to the lab first thing in the morning and they stain it for the tubercle bacilli, for 3 days straight. Chest radiographs also show lesions from PTB.
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This is false. \nWhite blood cells, also known as leukocytes, are the body's defensive cells and are part of the immune system. There are different types of leukocytes, including B lymphocytes and T lymphocytes.\nB lymphocytes msture in the Bursa of Fabricius. {hence their name}\nand also include two types:\n      a) Memory B cell- these cells "remember" how to make a certain antibody in response to a particular pathogen (antigen).\n      b) Plasma B cell- secrete antibodies in order to destroy antigens. antibodies bind the antigens together to make the easier targets for the phagocytes (which "eat" them up.)\n\nT lymphocytes mature in the thymus {that's what the T stands for}. There are three kinds of T cells:\n     a)Cytotoxic T cells destroy infected cells. \n     b) Helper T cells, when activated, they proliferate and secrete cytokines that regulate or "help" effector lymphocyte function. \n     c) Regulatory T cells, also known as suppressor T cells, suppress activation of the immune system and maintain immune system homeostasis. If these fail, you get an autoimmune disease (where the immune system attacks itself!)\n\n\nOn the other hand, Red blood cells, also known as eythrocytes, carry oxygen. They have hemoglobin, which is a globular protein containing four subunit proteins found in the blood of vertebrates (organisms with a backbone). The heme group has iron in it, and this is where the oxygen binds to. This also gives blood its red color.\nRBCS are circulated by the blood.\ntheir biconcave shape (like they have a dent on both sides...) let them carry oxygen more efficiently as well. \nA disease of this, called sickle cell anemia, is when RBCs are sickle shaped and do not carry oxygen efficiently, resulting in a tired person. \nyeah.\nhave a nice day!
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Seperating cells from Morula to use them for medical purpose is technically feasible. But at present seperating such cells is not feasible. Some more research is needed.
272384
The cell-mediated response involves cells that are specific to the antigens on the invading pathogens. These cells are called T cells. The T-cells develop surface receptors called T-cell receptors where they become programmed for the antigen of a specific pathogen.  Some of the T cells recognize and destroy foreign cells.  Hope this helps. I just had an exam on it and passed!!
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You could try to create a felixin knockout mouse in the mouse orthologue to human felixin to determine if the lack of expression in the mouse produced cat eyes syndrome.  If so, then you could test if subcloning the mouse felixin into an expression vector (for gene therapy-viral delivery), is therapeutically effective in the mouse.  Such animal work would be necessary before performing a similar experiment in human clinical trials.
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Complement mediation needs some amount of energy (created by Glucose utilisation)and so bactiriacidal activity is lower in less controlled diabetics.Complement inactivated serum does not need extra energy.I can not readily explain defference between C3 and  C4.Even plasma cells need effective glucose utilisation for optimal functioning.So IgG and IgA  are in higher quantity.
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http://cellbio.utmb.edu/cellbio/nucleus.htm\nhttp://www.cdli.ca/~dpower/cell/nucleus.htm\nhttp://www.cellsalive.com/cells/nucleus.htm\n\nDo some research, we're not here to complete your homework for you.
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You can find practical information from Qiagen website if you use their kits which are quite popular these days.  \n\nIt depends on which methods you use for isolation.  The alkali lysis (see link below) was commonly used to rupture bacteria.  Plasmid DNA (smaller in size and more soluble) is separated from baterial genomic DNA (larger and less soluble).  The plasmid DNA is then separate from proteins by phenol extraction where the proteins are removed to the phenol phase while plasmid DNA stays in the aquous phase.  The plasmid DNA is then precipated with ethanol to complete the purification.\n\nQiagen's kit and others overcome the use of phenol (which is toxic and smelly) by using a solid phase that bind DNA to seperate the contaminating proteins.  The DNA is later eluted from the solid phase to complete the purification.\n\nHere are additional links:\nhttp://biotech.biology.arizona.edu/labs/DNA_isolation_plasmid.html\nThe concept of alkali lysis method of plasmid DNA isolation is shown here:\nhttp://a32.lehman.cuny.edu/molbio_course/plasmid_protocol.htm
58087
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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Measurement of cell proliferation and cell mediated contraction in 3-dimensional hydrated collagen matrices \n\nSummary  This report describes simplified methods for the preparation of reconstituted collagen gels containing a uniform distribution of anchorage dependent cells in 96-well microtitration plates, their dissolution with collagenase allow harvesting of either cells or medium, and objective analytical methods for measuring cell mediated contraction of collagen gels and [3 H]thymidine incorporation rates.\nKey words  collagen - cell proliferation assay - contraction assay - micro cell-culture methods\n\nTo whom requests for reprints should be addressed at Opthalmic Research Unit, University of Western Australia, Royal Perth Hospital, GPO Box X2213, PERTh 6001, Western Australia.\n\n:>peace
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The correct answer is C.\n\nIn A. Only T-cells take part in cell mediated immunity. The others are not cell-mediated. For example, B-cells take part in humoral immunity. Natural killer cells are non-specific (innate immunity) and are therefore not part of cell-mediated immunity (which is acquired immunity).\n\nIn B. Infected cells do get killed off in the process. Infected cells will display the antigen fragments via their major histocompatibility  (MHC) I proteins on the surface of the cells. These antigens will allow cytotoxic T-cells to bind to them with their CD-8 receptors. The cytotoxic T-cells will release perforins that cause pores to form on the cell membrane. Granzyme is also released to cause proteins in the cell to break down.\n\nIn C. Antibodies are part of the humoral response (humoral immunity). Opsonization only occurs for antigens outside the cell, in the bloodstream or lymph fluid. They are not part of cell-mediated immunity.\n\nD is definitely wrong.
564781
isolate the pathogen...
496874
Have you tried this site\nhttp://www.answers.com/topic/elisa