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Immune Response (and Chicken Pox)
Transcript of Immune Response (and Chicken Pox)
Airborne disease; coughing, sneezing, sharing food, etc. by infected person can spread the disease
Direct contact with the fluid from chicken pox blisters can also spread the disease
Those who never had chicken pox and never got the chicken pox vaccine before gets the disease ** Varicella Zoster Viruses enter the human host. So... As a response to the foreign wave of VZVs, different antigen-presenting cells (APCs), undergo phagocytosis and engulf the VZVs. http://www.buzzle.com/img/articleImages/275750-33110-45.jpg Antigen Presenting Cells (APC) B Cells Cytotoxic T-lymphocytes (CTLs) T-Helper Cells Antigens will enter a host's body through inhaling, ingesting and such, and it is the APC's job to stimulates the T and B lymphocyte activities to terminate the antigens.
APCs engulf the antigens or sometimes the cells wit hthe antigens. This helps in the termination process of the antigens.
There are many different types of APCs, and the main ones are macrophages, dendritic cells, and B cells.
APCs will usually recognize the antigens by their PAMPs and TLRs. After they recognize the foreign antigen, they engulf the foreign antigen. The antigens will be contained in endosomes, and a lysosome in the cytoplasm will come around and break the the antigens. While this is going on, the APCs will be producing the MHCs simultaneously in the endoplasmic reticulum. The APCs will then present the bits of antigens that it broke down in the endosomes on its membrane surface with the MHC II complexes. Though there are measures by the body's immune response to suppress the infection, some cells do get infected by the viruses or other pathogens. This is why the body needs CTLs.
Hemapoietic cells from the body's bone marrow gets transferred to an organ called thymus, and there, the progenitor cells are developed into CTLs.
CTLs are unqiue from other T-cells because it contains the CD8 co-receptor, a transmembrane protein that specifically aids CTLs' function.
As an infection get's detected, mature CTLs can be recruited by other cells such as T-helper cells (Th 1), B Cells, and Dendritic Cells. This is usually done by CTLs picking up the emission of cytokines.
At the infection site, the cells would have been infected by the viruses or pathogens, and when these pathogens enter the body, bits of the viral or antigenic protein will be displayed on the infected cell's MHC I complex. Only nucleated cells have the ability to produce MHC I complex and display the foreign antigen, however.
The recruited CTLs will eventually gather around the infection site and find the infected cells. They will then bind to the infected cell's MHC I complex (with the foreign protein displayed) with their T-cell receptors (TCR) and CD8 co-receptors. The T-cell receptors will bind to the foreign bits of antigen that is being presented by the infected cell, and the CD8 co-receptors will bind directly to the MHC I complex to hold the infected cell and the CTL together so the activation of CTLs can occur successfully.
Once the CTLs recognize that the cell has been infected, CTLs take actions to kill the infected cell, and one way they can do this is by releasing granzymes and perforins. Perforins, cytolytic proteins, are released from the CTLs and attaches to the membrane of the infected cell. Then, the perforins cause the formation of pores that lets substances travel into the infected cell. CTLs will then release type A and type B of serine proteases called granzymes. Granzyme A will enter the cell through the pores that perforins created, and cleave the NADH dehydrogenase in the cell's mitochondria. Granzyme B will induce procaspase 3 cascade. Both will cause apoptosis of the cell.
Another way the CTLs can kill the infected cells is by using the Fas ligands. Fas ligand proteins of the CTLs can bind to the Fas receptors of the infected cell. This will induce the recruitment of procaspase 3 around the Fas recepotrs in the infected cell, and the infected cell will die through apoptosis due to the cleavage of the procaspases. T-helper cells serve a critical role in the body's immune system by recruiting necessary immune cells for the termination of the antigens to occur.
Like the CTLs, T-helper cells are developed in the thymus with the hemapoietic cells from the bone marrows.
Unlike the CTLs, T-helper cells have the CD4 co-receptor that is unique the the T-helper cells. T-helper cells also have the CD3 co-receptors that aid the binding process.
There are different types of T-helper cells that are separated by their functions in the body.
For the T-helper cells to function, there has to be an APC that has lysed in a pathogenic antigen, broken it down and displayed it on its MHC II complex. This interaction generally happens in the lymphnodes.
Like the CTLs, naive T-helper cells will bind to the foreign piece of antigen with its TCR and CD3 co-recepters, and the CD4 co-receptors will come around and bind directly to the MHC II complex to hold the two cells together.T-helper cells are antigen specific. This means that certain T-helper cells can only respond to specific antigens and not others.
When the T-helper cells get activated to their specific antigens, they take action by releasing cytokines that will help with the recruitment and eventual termination of the infectants. Different types of T-helper cells secrete different cytokines to serve different functions. For example, Th1 cells secrete substances such as interferon gamma to promote phagocytosis of macrophages. Th1 cells also release cytokines that recruits and activates CTLs. Th2 cells secrete interleukins 4, 5, 10, 13 that promotes IgE antibody production and self reproduction, and activates eosinophils.TFH cells assist B cells in their transformation to plasma cells.
Some T-helper cells, after getting activated, are turned into memory T-cells that can act effectively against future infections with the identical antigens. B cells are a crucial part of the body's immune response. The B cells will produce antibodies that can neutralize the antigens are terminate the infection.
B cells are developed in the bone marrow. B cells are made from progenitor cells in the bone marrow called pro-B cells or pre-B cells. These cells go through the development process, and their B-cell receptors are developed during this process.
B cells are very antigen specific and only react to the antigens that they are built to react to.
B cells are activated by the T-helper cells that carry the antigens from the APCs. The T-helper cells will bind to the B-cell receptors with their T-cell receptor and CD4 co-receptors. During this activation process, T-helper cells release cytokines that help the B-cell multiply in number.
The B cells can either turn into plasma B cells or memory B cells. Plasma cells are the activated form of B cells that secrete the antigen specific antibodies that will suppress the infection. Memory B cells will stay in the body for a very long time and will take action when the same infection happens in the body later in time. Different types of B cells exist, and they produce five different types of antibodies: IgM, IgD, IgG, IgA, and dIgE. The cells necessary for immune response such as B cells, T-helper Cells and CTLs are all developed in the bone marrow. Hematopoietic stem cells from the bone marrow will be transerred to the Thymus for T-cell development. The progenitor cells will then go through a complicated process of selection that will result in either T-helper cell or CTL. Progenitor cells do not have the capability to produce CD4 or CD8 coreceptors initially, but it eventually develops the ability to produce both coreceptors. Then, in a selection process, some T-cells will lose its ability to produce CD8 and some will lose its ability to produce CD4. This results in the T-helper cells with the CD4s and CTLs with the CD8. Source: http://en.wikipedia.org/wiki/File:B_cell_activation.png http://www.biologyreference.com/images/biol_03_img0247.jpg APCs engulf the antigens, will break down the antigens, and present it with their MHC II complexes. http://www.blobs.org/science/cells/acquired2.gif Diffferent T-helper cells in the lymph nodes will the bind to the APCs and become activated. (Activation occurs after the CD28 binding.) The different T-helper cells will then release different types of cytokines that promoted the neutralizing of these antigens and infected cells. The reason that people who once had the disease does not suffer from chicken pox again is because the memory T-cells and memory B-cells will recognize the disease and stop it from spreading before the symptoms of disease shows. T-helper cells will approach the B-cells, and the B-cells that are capable of fighting VZV viruses will be activated by the T-helper cells. Most of the B-cells will become plasmid B-cells and secrete antibodies against the VZV virsuses, and some will become memory B-cells and store the information to fight the infection if it occurs again later on. http://www.nature.com/nrmicro/journal/v6/n7/images/nrmicro1930-f4.jpg Though there are measure taken in order to stop the viruses from spreading around, cells will still get infected by the VZV viruses. The infected cells will present the peptides of VZV vrisues on their MHC I complex. (Not shown in the picture) http://www.nature.com/nrmicro/journal/v6/n7/images/nrmicro1930-f4.jpg http://www.ncbi.nlm.nih.gov/books/NBK26926/figure/A4499/?report=objectonly Cytotoxic T-lymphocytes will be alerted by cells such as the T-helper cells (Th1). They will be recruited to the area of infection and then kill the infected cells. They can either kill the infected cell by using perforin and granzymes, or they can use the Fas ligands. Both will induce apoptosis and cause the infeted cell to die.