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About this sample
About this sample
Words: 604 |
Page: 1|
4 min read
Published: Jan 29, 2019
Words: 604|Page: 1|4 min read
Published: Jan 29, 2019
MHC class I molecules present peptides which bind to the T cell receptors of cytotoxic T lymphocytes. These are found on the cell surface of almost all nucleated cells in the body which enable the T cells to distinguish between “self” and foreign antigens. This interaction also involves the binding of a CD8+ T cell surface glycoprotein to the MHC (class I) molecule (McDowall, n.d.).
MHC class II molecules however, display peptides which are recognised by helper T lymphocytes. It is only specialised antigen presenting cells that express MHC class II molecules, which primarily consist of dendritic cells, macrophages and B cells. The binding of helper T cells to MHC class II molecules also involves the binding of a CD4+ T cell surface glycoprotein. It is the difference in the CD8+ and CD4+ glycoprotein receptors that allow these two subsets of T lymphocytes to be distinguished.
When T cell receptors bind to the antigens presented by MHC molecules a signal transduction takes place which induces a response of the T lymphocyte. Helper T cells Helper T cells (also known as CD4 T cells) are not directly involved in attacking pathogens or infected cells however they are extremely important as they are required for nearly all adaptive immune responses. Naïve T cells are activated causing them to mature, proliferate and coordinate immune responses by secreting cytokines which act on other immune cells. There are two main types of T helper cell, categorised based on their profiles of cytokine secretion, which determine their functions:
Type 1 (TH1) cells primarily secrete the cytokines interleukin (IL)-2 and interferon-gamma (IFN- γ). They participate in cell-mediated immunity and activate macrophages, antibody production and cytotoxic T lymphocytes. They can also cause delayed type hypersensitivity (DTH). Type 2 (TH2) cells secrete cytokines IL-4, IL-5, IL-10, and IL-13 which help B cells in promoting the synthesis of Ige antibodies as well as activation of eosinophils, mast cells and deactivation of macrophages.
The two cell types also differ by the type of immune response they coordinate. TH1 cells generate immune responses against intracellular pathogens such as bacteria and viruses whereas TH2 cells respond to extracellular pathogens such as helminths (Perkel, 2001). Helper T cells also bind to B cells and secrete lymphokines which activate the B cells stimulating them to differentiate into plasma cells and produce
Neutrophils and macrophages of the innate immune system serve as the first line of defence to pathogenic invaders. However, some of these pathogens cannot be recognised so a more specific approach from the adaptive immune system is required to eliminate them (Janeway, 2001). There are two divisions of acquired (adaptive) immunity, the humoral response which is mediated by antibodies and the cell-mediated response whereby T lymphocytes play a central role. Antibodies are only effective against extracellular pathogens, once pathogens enter the host cells they can evade the humoral immune system which is when cell-mediated immunity acts to defend the body against intracellular pathogenic microorganisms (Silverthorn, 2015).
T lymphocytes (T cells) originate in the bone marrow before migrating as thymocytes to the thymus where they mature, multiply and differentiate (Khan, 2012). During their development, T cell receptors are inserted into the cell membranes. These receptors bind specifically to major histocompatibility complex (MHC)-antigen complexes found on the surface of antigen presenting cells. The function of MHC molecules is to bind to peptide fragments derived from digested pathogens and to display them on the extracellular cell surface allowing recognition by T lymphocytes. Through the recombination of genes that encode the T cell receptors, the body carries a surplus of T cells, each with different specific T cell receptors allowing quick immune responses to invaders (McDowall, n.d.).
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