Summary: Adaptive Immune Response

“Humoral immunity is a type of immune response that depends on antibodies.” The response begins when a pathogen binds to a B cell. The B cell will engulf the pathogen and display a part of the antigen on its exterior. Once a T cell is exposed to the antigen-presenting B cell, the T cell will release proteins to activate the B cell. Now that the B cell is activated, it will produce antibodies to cause the pathogens to clump together. In the last stage of humoral immunity, phagocytes will engulf and destroy the pathogens.

The human immune system creates a series of responses in the body to defend the body. If a foreign organism, such as a virus or a cold invades your body, it recognizes these foreign organisms, and, in turn, attacks them to get rid of them. One can think of the immune system as an army of many cells which have set up their own bastion in the human body. They have only one job: To defend. The immune system’s cells are various kinds of white blood cells. The human body typically creates about 1000 million white blood cells on a daily basis. A group of these cells, macrophages, establish a patrol of sorts throughout the body killing germs as soon as they enter the body. However, sometimes an infection can cause the macrophages to succumb to it. The body begins to fight back with stronger T- and B-cells.

Instead of being recognized and attacked by T cells, bacteria are recognized and attacked by complement proteins. “Complement proteins assist in bacterial killing via three pathways, the classical complement pathway, the alternative complement pathway or the lectin pathway. The first steps of the classical complement pathway require the binding of antibodies to the surface of the target bacterium” (Immune, 2016). At this point, the antibodies are handled by protein complexes which bind to the surface of the invader (much the same as the process of T cells in viruses). In other words, the body goes through a similar reaction of identifying and then attempting to destroy the invader, including the formation of a membrane attack complex. “MAC can insert into the cell membrane of Gram-negative, but not Gram-positive, bacteria. There, it produces pores that allow the entry of membrane damaging molecules, such as lysozyme, and makes the bacterium susceptible to osmotic lysis” (Immune,

When foreign invaders such as bacteria or viruses enter the body, immune cells called lymphocytes respond by producing antibodies, which are protein molecules. These antibodies fight the invaders known as an antigen and protect against further infection. A primary immune response happens the first time a person is exposed to an antigen. This response is slow and takes several weeks to occur, memory cells

The main aim of the immune system is to limit and dispose any harmful waste products as well as evacuating the damaged tissues so that the body can begin healing. The body’s self-protective reaction comprises of variations in the blood stream to take in an increased discharge of fluids from the veins together with an increase of plasma, T-lymphocyte cells, proteins and phagocytes to enter the tissue so as to heal the damaged area as well as fighting off bacteria and viruses. The T and B cells are the most important cellular elements of the adaptive immune response. When a person is stressed, the ability of the immune system to attack antigens is usually reduced and one becomes more vulnerable to infections. T and B cells may play a significant neuroprotective role in both stress and inflammation. Through their

The consequence of these interactions is an adaptive immune response of antigen-specific lymphocytes to the antigen, as well as the development of immunological memory. Adaptive immune responses are generated by clonal selection of lymphocytes, and are distinct from innate responses. The immune response consequence is in result to the antigen

Previous studies have shown that killer T cells that protects us from bacterial damage plays a major role in the

Similar to T cells, each B cell also has its unique B-cell receptor that recognizes a particular antigen to be selected and eventually to become activated. The activated Th2 sends signal (interleukein – 4 B Cell Growth Factor) to the activated B cells to make more clones of the B cells. Once the B cell produces enough number of its clone, B cells start to express another receptor for Th2 to send another signal (B Cell Differentiation Factor or interLeukin-5). Once the B Cell Differentiation Factor stimulates B cells, they become plasma cells and start the production of IgM initially and then IgG. Some of B cells, however, become memory cells instead of becoming plasma cells. The amount of the antibody produced at the first response to the toxoid molecule is usually relatively low and it takes about 2 to 3 days (but often is longer, as long as weeks) for the B cells to be activated and to be differentiated into plasma cells. The first antibodies that encounter toxoid is, as mentioned previously, is IgM and a small amount of IgG. After about a week, however, the number of IgG supersedes IgM. Overtime, antibody level

Humoral immunity helps the body protect itself, the humoral immune response is by antibody molecules that are secreted by plasma cells. They produced antibodies that target foreign material in the blood stream that is seen as potentially dangerous, marking it for destruction. B-lymphocytes play a major role humoral immunity, they help the immune system in the fight against infections because of antigen presenting cells. They are the class of immune cells that synthesize antibodies and are responsible for humoral immunity. When the antibodies react with millions of potential antigens, the immune system does not have full capacity to create antibodies that react with millions of antigens.

When an antigen is detected, several types of cells work together to recognize and respond to it. These cells trigger the B cells to produce antibodies. Antibodies and their responding antigens fit together like a key and a lock. Although antibodies can recognize an antigen and lock onto it, they are not capable of destroying it without help. That is the job of the specific T cells, also called “killer cells”. The T cells are part of the system that destroys antigens that have been tagged by antibodies or cells that have been infected or somehow changed. T cells are also involved in helping signal other cells of the immune system to do their jobs.

Humoral immunity is characterized by secretion of proteins called antibodies, which immobilize and block the ability of pathogen to infect the host cells in additon of promoting the ingestion by phagocytes. Antibodies are secreted by B-lymphocytes, which are derived from bone marrow and on activation of antigen differentiate into plasma cells known for their ability of antibody secretion. Humoral immunity is defense mechanisam used against extracellular microbes and toxins, since antibodies can bind to them and assist in their elimination. Antibodies are specific for antigens found on microbes and, as previously said, recognize fine differences between the

After the APCs have been loaded with the vaccine-generated antigen, they travel to the secondary lymphoid organs, where they activate naïve T-cells through a combination of MHC, co-stimulatory molecules and TCR. Once CD4+ TH cells are activated, they secrete cytokines “during cell-to-cell interaction with B cells and bind to

This include the phagocytosis process which include white blood cells. This white blood cells take over the pathogens and tries to fight them back. The macrophages, eosinophils and neutrophils work to try to get fight the pathogen. The process starts by white cells recognizing the pathogen. Then the white cells adhere to the pathogens and don’t allow them to attach. Lastly white cells try to break the pathogens out by the help of the enzymes. This can also not work because some pathogens may have more protection and may not allow the enzymes to break them out. Another thing that can happen is your compliment systems may kick in and a person can get fever which tries to make the pathogen uncomfortable and some bacteria may even get kill since some are sensitive to heat. Also you may get an inflammation, which are extra white cells that are put in an area that needs them. When the blood vessels expand it can allow movement of fluids. Inflammation can also help us but can also be harmful because if inflammation occurs in place where there isn’t much room, then it can damage your central nervous system. If none of this things work then the third line of defense comes into play. The process is a specific immune response. It starts by the microphage reading and does an antigen presentation. Then the B-Cells produce antibodies that are specific to a pathogen. Does antibodies then

If a pathogen breaches barriers: innate immune response result into an immediate effect of non- specific response. All Innate immune systems derived from plants and animals, when a pathogen evades the innate response, a third layer of protection is possessed by vertebrates in which activation of adaptive immune system takes place. The immune system response adopts itself within an infection and pathogen recognition is improved. As a result of the improved response, its then retains itself when the pathogen is eliminated in form of an immunological memory and allows the adaptive immune system to mount faster and stronger when pathogen is encountered each time.

On the other hand, the immune system of a person with CD would bring the gliadin complex past the defence barrier on the epithelial lining. The epithelial lining is usually in close contact to prevent pathogen from getting past the barrier; however in CD, the cells do not follow the normal mechanism. A macrophage cuts the gliadin and expresses it on the cell surface with MHC II molecules. The role of a macrophage is to maintain immunity by selectively sampling materials in the body by distinguishing self from foreign material via phagocytosis. MHC II molecules vary for different antigens, hence for gliadin, HLA-DQ2 and HLA-DQ8 molecules are expressed on the surface of the macrophage. The presence of these MHC II molecules attract another set of cell that will lead to inflammation of the epithelial cells, and the production of autoantibodies against gliadin. The inflammation will attract killer cells to the site, which will induce death on the epithelial cells. Due to the destruction of the epithelial lining, gaps will form, allowing more gliadin to pass through the barrier; this will produce a positive feedback as more autoimmune activity and the destruction of epithelial lining persist.