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Immunology-APC, CD4, CD8, and B cells

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Risun Udawatta

on 2 May 2011

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Transcript of Immunology-APC, CD4, CD8, and B cells

APC, CD4+, CD8+, and B Cells Our Immune System begins with our innate immune response. The Innate Immune Response begins when a foreign invader enters into the cell.Mast cells and blood platelets are naturally found in the tissues of our body.Mast Cells release cytokines, TNF-alpha, chemokines, and IL-1. These molecules dilate the blood vessels so that the endothelial cells can tether neutrophils and macrophages into the tissue. Blood platelets release blood clotting proteins to a) stop bacteria from entering into the body, and b) to stop the body from bleeding out. Once neutrophils and macrophages are in the tissue, they start to engulf antigens, bacteria, and infected cells. Neutrophils only kill these molecules and cells, while macrophages are the bridge to our bodies adaptive immune response. In general, macrophages engulf these cells, release cytokines, and initiate tissue repair. http://www.uic.edu/classes/bios/bios100/lecturesf04am/inflammation01a.jpg APC's, or anitgen presenting cells, are the bridge to the adaptive immune response. APCs are macrophages, dendritic cells, and B cells. Like the name says, APCs present anitigens to the adaptive immune response. Once APCs have presented the antigens, the adaptive immune response will start to create antibodies to inhibit antigens, bacteria, and/or viruses. APC begin their process of presenting antigens when PAMPS are detected by the APCs. The PAMPS will attract the APCs to the infected cells, antigens, and/or bacteria. For bacteria infections, macrophages and dendritic cells will engulf the antigens and bacteria. For viral infections, dendritic cells can only engulf the infected cells. For bacterial infections, an antigen will be engulfed by an APC. TLR, toll like receptors, will attach to the antigen, and endocytosis will occur. Once the antigen is engulfed, the pH of the engulfed vesicule lowers so that the antigen denatures. Then the engulfed vesicule fuses with a lysosome, and the antigen further degrades. In the endoplasmic reticulum, the MHC Class II complex is being matured. Once the MCH class II complex is made, the engulfed vesicle will attach to the endoplasmic reticulum. A part of the antigen will attach to the MCH class II complex. Then this molecule will bleb to the membrane. After an APC cell presents the antigen on its membrane, a CD4+ cell will attach to the APC. This attachment is called an immunological synapse. For CD4+ cells to take the antigen, two signals must be made. The first is when a CD4 protein on the CD4+ cell attachs to the MHC class II protein and when the T cell receptor attaches to the antigen. The other signal is when a CD28 and CD80 molecule attaches to the APC. Once these two signals are met, the antigen is taken by the CD4+ cell. Once the CD4 cell takes the antigen, it becomes activated. At this point, the CD4 cells can either turn into memory T cells (TH1) or activate B cells (Th2). Th2 cells are the cells that activate B cells. The CD4 cell will release IL-2 and IL-4. These cytokines, will make the cell turn into a TH2 cell. Once it is a TH2 cell, it will release IL-4, IL-6, and IL-10 which activates B cells. Th1 cells will occur, when CD4 cells dont recieve IL-2. Once they are Th1 cells, they will proliferate and turn into memory T cells. Once a B cell is created, it acts like an APC cell. It will engulf an antigen, digest it, and present it on its membrane just like an APC cell would. Once the antigen is presented on the cell, a T helper cell, CD4+, will attach to it. Once this occurs, IL-2 will be released by the t helper cell, inducing the B cell to proliferate and differentiate. Most B cells will turn into plasma cells, but a select few will turn into memory cells. Plasma cells are the cells that produce antibodies to neutralize anitgens. This occurs by BDG recombination in the cell. Different combination of antibodies will be created until one antibody works best against the antigen. This antibody will be the antibody stored in a memory cell, if the body is infected with the same bacteria. Plasma cells will continue to release antibodies until the antigens and all the bacteria die. For Viral Infections though, our immune system responds a little differently. To explain the immune response for viruses, I will explain the immune response that our bodies have when we are infected by the Varicella Zoster Virus, commonly known to cause chicken pox. For viral infections,the immune response is the same, except for a couple changes. The innate immune response is the same. Except that macrophages wont engulf antigens, but this time infected cells. APCs will degrade the infected cells, and present an protein on its membrane from the infected cell. The biggest differences in viral infections, is that CD8+ is the major combatent. CD8+ is activated when T helper Cells attach to APC's. IL-2 is released from CD4+, which activate CD8+. CD8+ is considered to be a killer cell. It detects infected cells by the protein on the MHC Class I complex. MHC class I complex is found on all cells that have nucleus. MHC class I complex is a protein that is supposed to portray the cell proteins. An infected cell will have wrong proteins on the MHC class I. CD8+ will detect this and kill the cell. CD8+ cells attach to infected cells by the MHC class I complex. This is immunological synapse between an infected cell and a CD8+ cell. Once CD8+ attaches to the infected cell, perforin and granzymes are released from the cell. Perforin creates pores in the membrane, while granzymes break down proteins. The granzyme will initiate apoptosis, which will lead to the eventual death of the infected cell. When Varicella zoster virus (VZV) infects our body, the innate and adaptive immune response is intiated. CD8+ cells kill infected cells, while B cells create antibodies to specific proteins the virus creates. CD8+ cells can recognize many proteins made by VZV, and successfully kill the infected cells. IgG, IgM, and IgA are the main antibodies that B cells create to help fight the viral infection. These proteins can make cells lyse through antibody-mediated-cellular cytotoxicity. Other proteins that can also fight this infection are gE and gI proteins, which neutralize VZV activity in the cell. (Arvin, 1996) Arvin, A.M. (1996). Varicella-zoster virus. Clinical Microbiology Review, 9(3), 361-381. Campbell, N.A., Reece, J.B. (2008). Biology. San Fransico: Prentice Hall. Campbell, N.A., Reece, J.B. (2008). Biology. San Fransico: Prentice Hall. Campbell, N.A., Reece, J.B. (2008). Biology. San Fransico: Prentice Hall.
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