Question

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Acquired immune responses are capable of controlling an infection, however, the acquired immune response is controlled itself through different mechanisms. It is primarily activated by a threshold level of antigen that is produced through the defensive action of the innate immune system. Pathogens and antigens interact and cause dendritic cells to activate to become antigen-presenting cells. Then, the antigens are transported to the lymphoid organs by the antigen-presenting cells. After several days, antigen-specific T cells and B cells locate the foreign antigen, and ultimately differentiate into armed effector cells. These cells either leave the lymphoid organ to go to the sites of infection or stay within the organ to promote humoral immunity. The path the effector cells take is dependent on the differentiation of CD4 T cells. There are two different subsets of CD4 T cells, Th1 and Th2. The function of Th1 is to activate macrophages, while Th2 works to activate B cells, especially during the primary response. Both of these CD4 T cell subset are capable of regulating each other, which is essential done by the cytokines of each respective T cell type. Ultimately, the effector cells remove the pathogens to control the infection (1). Once an infection is effectively under control, it is critical to remove the effector cells to allow for the restoration of the tissue. The immune system has mechanisms in which it is capable of removing these cells. When effector cells are no longer needed, they undergo apoptosis. The function of effector cells is to remove the stimulus that activated them, but when that stimulus is gone, the effector cells no longer have anything to remove except for themselves, which occurs through apoptosis. Apoptosis causes cells to die, and they are subsequently removed through macrophages. They are capable of identifying the dying cells through the composition of their membrane, specifically the lipid phosphatidylserine. In a normal cell, the lipid is found on the inner portion of the plasma membrane. However, when a cell undergoes apoptosis, it redistributes to the outer surface which allows for easy recognition by phagocytes. While some effector cells are removed, some are retained to allow for formation of memory T-cell and B-cells (1). The acquired protective immune response is critical in providing protection against pathogens. It is acquired through effector T cells or antibodies that are generated when exposed to the pathogen, as described above. This can be done by initial infection or through vaccination that allows for immunological memory. The specific pathogen involved influences the type of effector T cell or antibody that provides protection. For example, the polio inactivated vaccine utilizes preexisting antibodies (IgA) to neutralize the virus and prevent its spread of infection (1). These antibodies are known as IgA, and are produced within the gut mucosa. In order to activate the mucosal immune response, antigens are transported across the epithelium through the use of microfold (M cells). They are then presented to effector B lymphocytes that result in stimulated B cells to migrate to distant mucosal cites. This ultimately leads to the production of IgA that neutralizes the antigen. The neutralization of these substances prevents it from binding to receptors within the tissue. Therefore, the neutralized antibody-antigen complex formed is ultimately removed and destroyed by macrophages (2).

Answer 1

Acquired immunity is the immunity that a person gets during the life by acquring the disease or by taking a vaccination against a specific pathogenis disease.

The entry of disease germ which acts as an antigen stimulates the body to produce for immune activity when it is at threshold level. The disease germs when enter interact and cause dendritic cells and activate to become antigen presenting cells. The antigens are transported to lymphoid organs.

Secondary lymphoid organs provide sites for interaction of lymphocytes with antigen, which then proliferate to become effector cells. The antigen specific T-cells and B-cells locate the foreign antigen.

Both B-cells and T-cells are lymphocytes that are derived from specific type of stem cells, called multipotent haemopoietic stem clls in the bone marrow.

B-cells move to lymphatic system to circulate through the body and encounter an antigen which starts maturation process of B-cells. B-cells have a number of distinctive surface antigen-specific receptor

when a naive B-cell encounters an antiugen that fits or matches its membrane bound antibody, it quickly divides in order to become either a memory cell or an effector B-cells called plasma cells. Antibodies can bind to antigen directly.

T- cells once formed in bone marrow migrate to thymus to mature. the developing T-cells start to express. T-cell receptors (TCRs) and other receptors called CD4 and CD8 receptors. T-cell receptor can only recognize antigens that are bound to certain receptor molecules called MHC I and MHC II. MHC (Major Histo Cpmpatibility ) molecules are membrane bound surface receptors on antigen presenting cells like dendrtic cells and macrophages.

CD4 and CD8 paly role in T-cell recognition and activation by binding to either MHC I and MHC II.

CD4 are two kinds- Th 1 and Th 2. Th-1 activate macrophages and Th-2 activate B-cells during primary response.

After the function, some of the effector cells are removed by apoptosis. Apoptosis is a programmed cell death due to biochemical events that lead to the death of the cell. Some effector cells remain as memory cells which have a role in secondary immunity to intensify the response action.

The antigen -antibody complex formed during the immunity response to protect the body from invading antigens is ultimately removed and destroyed by the macrophages.