Danger Signals

The immune system depends on the body’s structures to help it function. For instance, the skin acts as the “body’s first line of defense.” If a pathogen finds a breach in the skin barrier, it is the circulatory system that must now signal the immune system of the invader. Shortly after, white blood cells will be notified of the infection and will target and destroy the pathogen.

The innate and adaptive immune response start with exposure to an antigen in the epithelium of

a. This function is mediated by T cells and B cells (memory cells) in our body via adaptive immunity. The adaptive immune system evolved in early vertebrates and allows for a stronger immune response as well as immunological memory, where each pathogen is “remembered” by a signature antigen. The adaptive immune response is antigen-specific and requires the recognition of specific “non-self” antigens during a process called antigen presentation. Antigen specificity allows for the generation of responses that are tailored to specific pathogens or pathogen-infected cells. The ability to mount these tailored responses is maintained in the body by memory cells. Should a pathogen infect the body more than once, these specific memory cells are used to quickly eliminate it. So basically killer T cells will identify antigens present on foreign cells. These antigens are not found in any of the cells inside our body. Therefore, T cells will identify them and kill them.

This is immunity in an organism that’s a result from the production of antibodies or lymphocytes after an antigen is identified in the body.

Human beings are born with immunity as well as they acquire it from the environment they grow in. Human innate immunity is assigned the task to hinder the harmful substances from entering the body. These immunity barriers develop a defense line. The innate immunity includes cough, tear enzymes, mucus, skin and the stomach acid. Hence, the role of innate immune system is to stop harmful materials from entering our body. In case the innate immunity is insufficient to fight, there is acquired immunity that fights harmful substances by getting exposed to various antigens. The acquired immunity is developed against specific antigen. Its role is to fight

The organs that make up the lymphatic and immune system are the tonsils, spleen, thymus gland, lymph nodes, and lymphatic vessels. White blood cells (leukocytes), red blood cells (erythrocytes), plasma, and platelets (thrombocytes) make up the blood. Lymphocytes are leukocytes (white blood cells) that help the body fight off diseases. Two types of lymphocytes are B cells and T cells. Lymphocytes recognize antigens, or foreign substances/matter, in the body. Lymphocytes are a classification of agranulocytes, or cells (-cytes) without (a-) granules (granul/o) in the cytoplasm. B cells are created from stem cells, which are located in the bone marrow. B cells respond to antigens by becoming plasma cells. These plasma cells then create antibodies. Memory B cells produce a stronger response with the next exposure to the antigen. B cells fight off infection and bacteria while T cells defend against viruses and cancer cells. A hormone created by the thymus gland called thymosin changes lymphocytes into T cells. The thymus gland is active when you are a child and slowly shrinks, as you get older. T cells bind to the antigens on the cells and directly attack them. T cells secrete lymphokines that increase T cell production and directly kill cells with antigens. There are three types of T cells: cytotoxic T cells, helper T cells, and memory T cells.

Dendritic cells are known as the gatekeepers and are critical to an immune response. Dendritic cells can either have an immune response or induce tolerance because of the production of different mediators and surface molecules. Because dendritic cells can promote differentiation of CD4+ cells into other types of T-helper cells they can further shape the immune response. What type of response is dependant on the mediators produced and then further influenced by cytokines from the surrounding environment. T-helper cells activate inflammatory cells and form the allergic reactions that are crucial through cytokine production. The allergen specific B cells are engaged by the T-cell receptors on the Th2 cell surface leading to production of IL-4, IL-3 that allows switching in B cells and the synthesizing of IgE (Faoud 2011). The allergen specific B cells and Th2 cells become memory cells for future immune

Humoral immunity also known as the B cells becomes mature in the bone marrow. Humoral immunity lymphocytes produce antibodies, which bind directly to the surfaces area of an antigen and label it for destruction. Cellular immunity also known as T cells originally made in the bone marrow but mature in the thymus. Cellular immunity do not produce antibodies, it relies on the production of cytotoxins, which is produced by T-lymphocytes and natural killer cells.

T cells are part of the adaptive immunity that proliferate in the thymus, their protein antigen receptors provide pathogen specific recognition

When it attaches to an antigen, it reels that antigen in and clones itself and makes an army of B lymphocytes to fight at one specific antigen. Some become Effector cells, Memory cells, or more B lymphocytes. The humoral response allows your body to achieve immunity by encountering pathogens either randomly or on purpose. The last and final defense are called the Cellular immune response. There are different names for these types of white blood cells and they are called T cells. The different type of T cells is Helper T cells, Cytotoxic cells, Memory T cells, Suppressor T cells, regular and lastly, Neutral killers. Helper T cell can’t fight diseases but can call other cells that can fight diseases. Cytotoxic cells can kill diseases or cells that are infected or cancerous. Helper T cells use something called cytokines to alert other Helper T cells, which then make more Helper and Memory T

Studies have revealed that the P2X7 receptor may hold some of these answers (Ferrari et al. 1997), (Perregaux and Gabel, 1998). P2X7 is said to be a key mediator in the activation and secretion of the interleukin-1 family of cytokines. Perhaps the two most well established are the mechanisms involved with the maturation and release of IL-1β and IL-18. Muñoz-Planillo et al. (2013) suggests that rapid K+ efflux acts as a co-signal alongside activation of toll-like receptors via pathogen-associated molecular patterns (PAMPs). These two signals combined are said to initiate the assembly of the NLRP3 inflammasome. Whilst the signal received through toll-like receptors is responsible for the synthesis of inflammasome components and inactive forms of IL-1β and IL-18, the second signal received through rapid K+ efflux influences the assembly of the inflammasome itself leading to the activation of caspase-1. Caspase-1 processes and activates pro-IL-1β and pro-IL-18

Dendritic cells are antigen presenting cells that stimulate the adaptive immune response by presenting antigens to the T cells. They are derived from hematopoietic bone marrow progenitor cells as immature dendritic cells. These immature dendritic cells have pattern recognition receptors like toll like receptors that recognize specific chemical structures of foreign antigens or non-self-antigens. Once the immature dendritic cells recognize foreign molecules they drain to the lymph nodes as mature dendritic cells and present these antigens in form of a peptide-major histocompatibility complex to naïve T and B cells for activation of the

When John was first immunized with tetanus toxoid, dendritic cells first encounter the toxoid. Dendritic cell is a type of antigen presenting cell (APC) that can phagocyte and breaks down the pathogen into short peptides. The short peptides (antigen) then combine with MHC class 2 and are displayed on the surface of the APC. While this process is going on, the dendritic cell moves within the lymph channel to get to lymph node, where they can present the antigen to naïve T helper type 2 cells. (Th2). Each Th2 has its own unique T cell receptors (TCR) and only a particular TCR can bind to the antigen that is presented on APC with MHC class 2. Once APC finds the right TCR of Th2 (meaning CD4 binds to MH2 and the antigen binds to TCR), the

To account for the versatility of a human system, scientists are beginning to use co-culture cell systems. These are systems that combine two or more cell lines. These types of models are beneficial for studies because they show how a response in the body is more likely to occur. Following toxic exposures, cells signal to each other to elicit a response to control for potential damage. For example, when a nanoparticle is inhaled it enters the lung. Once here, depending on the size of the particle, it travels to the alveolar region (the area of the lung responsible for oxygen exchange with the blood). Once in this region, if the particle is toxic, our immune response is activated. This means that immune cells, like macrophages, move toward the particle and attempt to engulf it to prevent further toxic effects. Immune cells often release chemicals that signal to other cells that damage has occurred. These signals then elicit responses, such as an inflammatory response, and additional cells are

The next cells are the T cells. There are many different types of T-cells. One is the Killer T-cell. They can recognize invaders with feelers on the outside of the cell and if the cell is infected, it can destroy the cell. Another type is the helper T-cell. The helper t-cell functions more as support. It matures B-cells and tells them to make antibodies by secreting a protein. A helper t-cell also activates the killer t-cell. The last major t-cell is the memory t-cell. If you get sick, the memory t-cell will remember the antigen and will the immune system be able to defeat the same disease faster. The next cell is the Natural Killer Cell. These cells are lymphocytes that destroy viruses by releasing a protein that makes the affected cell “program” itself for death. The process it destroys itself is called apoptosis. (Kidshealth.org)