Identify And Explain The Importance Of Cytokines Response To Interleukins

A T cell are also referred to as T lymphocytes which are key cells of specific immunity as referenced by Krasner and Shors.

There are many different abnormal cells that occur in breast cancer patients, but some of the most common are interleukins. In normal patients, IL-2 cells cause proliferation of the T cells as well as differentiation of cytostatic T-lymphocytes, but in breast cancer patients the abnormal cell interferes will cell mediated immunity response. IL-6 cells are fibroblasts, macrophages and lymphocytes, but in cancer patients they promote tumor growth by upregulating antiapoptotic and angiogenic proteins in the tumor cells. IL-8 cells are a key factor in the inflammatory response, but in breast cancer

The immune system contributes to homeostasis as it protects and defends against invaders that pose a threat to the body’s balance. Homeostasis is an internal balance that is maintained by multiple factors within the body. The immune system is responsible for avoiding and limiting infections in the body. It prevents and heals damage that invading pathogens may cause to the body. In this way, it helps maintain homeostasis by eliminating pathogens and the imbalances they cause in the body. A first defense, known as the innate immune response, activates as soon as the body is infected. It is the same regardless of the invader. Examples include skin, chemical secretions, and linings.

The TH1 response is cell mediated and promotes inflammation while the TH2 response is an antibody response and anti-inflammatory. When excessive, the TH1 response can cause extensive tissue damage. TH1 responses are characterized by IFN-gamma production. IFN-gamma produces macrophage activity and causes B cells to create a coating of Abs. This creates a cell-mediated response. This is effective against invaders that are inside of the host cells. In a cell-mediated response, the APC phagocytizes the invader via macrophage, monocyte, or dendritic cell. Next, the antigen enters the lymphatic system via lymph node. The APC presents the antigen to T cells where the T cells recognize the antigen and cytokines are secreted to search and destroy

IL-2 has been extensively studied by the scientific community because of its known involvement in the immune regulation. Provided that it has known functions of the immune system, it can also be inferred and tried to discuss that it is more complex than simply recruiting all the cells needed to engage in the fight for the immune system.

In the first process, NK cells recognize the target cell through its cell surface receptors. Here the infected cells coated with immunoglobulin G (IgG) antibodies bind to the IgG specific receptors (FcγR) expressed on the surface of NK cells. This receptor-ligand interaction activates the downstream signaling cascade of NK cells, which direct them to destroy the target cell by a process called antibody-dependent cellular cytotoxicity. The second mechanism of recognition relies on the expression of killer activating (KAR) and inhibiting receptors (KIR) expressed on its cell surface. These receptors recognize a range of different molecules present on the surface of nucleated cells and regulate the functional outcome of NK cells. Once the activating receptor is engaged, a “Kill” instruction is issued to NK cells, that in turn activates perforin and granzyme mediated cytolysis. The “kill” signal, conversely, can be overridden when the signal is sent from the inhibitory receptor, a mode typically exploited by viruses in the suppression of NK cell-mediated cytotoxicity (Delves and Roitt, 2000). Other immune cells such as eosinophils, basophils, and mast cells also make a major contribution to the first line of defense mechanism. Basophils and mast cells contain IgE specific cell surface receptors (FceR) and exhibit high affinity for pathogens coated with the IgE antibodies. These cells are particularly important in the case of atopic allergies such as asthma and hay fever, wherein the allergen binds to IgE cross-links FceR and triggers the secretion of inflammatory mediators such as histamines and prostaglandins. Eosinophils, on the other hand, act as weak phagocytic cells and function mainly through the release of cationic proteins and reactive oxygen species (ROS) into the extracellular fluid. Collectively, these immune cells stimulate a rapid and

The primary function of skin is to form a physical and chemical barrier to the external environment, against injurious insults. Harmful stimuli such as micro-organisms, ultraviolet radiation, toxic agents or irritants evoke a complex response known as inflammation. Inflammation is an essential response in the protection against injurious insults. The five classical signs of acute inflammation are pain, heat, redness, swelling, and functional loss. These signs can be explained by the different phases that the inflammatory response generally follows dilation of capillaries to increase blood flow, vasopermeabilization, leukocyte recruitment elimination of pathogens or injurious stimuli and resolution of inflammation [85]. At the molecular level,

The adaptive immune response is the response of antigen-specific lymphocytes to antigen, it functions through a series of steps aimed at limiting or destroying a particular antigen. T and B cells primarily mediate the responses of the adaptive immune system as they obtain the characteristics of specificity and memory. There are two classes of adaptive immune response; humoral immune response and cell mediated or antibody immune response. In order for the adaptive immune response to know when to respond, how

Cytokines are cell signaling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection, and trauma. Researchers at UC Davis have found that early exposure to inflammatory cytokines can “paralyze” CD4 cells. This CD4 paralysis could play a role in preventing autoimmunity. Autoimmunity is misdirected immune responses that can cause the immune system to go awry and attack the body itself. By shutting down CD4 cells, it prevented an autoimmune response. This research shows the potential to paralyze the immune system to prevent autoimmunity, or to adjust and teach it to accept transplanted cells and

They have rapid effector function and produce large amounts of IFN-, IL-4 and IL-5 within hours of antigenic stimulation (Lanzavecchia and Sallusto, 2000).

The immune system protects the body. It is made up of a network of cells, tissues and organs that work together to protect the body.

Inflammation is the localized immune response to tissue damage, injury, or infection. It is characterized by warmth, redness, swelling, pain, and loss of function. There are two types of inflammation: acute and chronic. Acute inflammation usually lasts a few hours to a few days while chronic inflammation lasts weeks or even months. There are a string of diseases and cancers that are possibly linked to inflammation. The inflammation can initially be acute, but if unresolved can lead to chronic inflammation which could ultimately progress to serious diseases, carcinogenesis, or tumorigenesis. Research has been conducted to figure out and understand totally the role of inflammation, inflammatory cells, and inflammatory mediators in certain diseases and cancers.

Inflammation can be the first response of living tissues to injury, infection or irritation (Saima Jalil, 2003) and could appear due to microbial infections, physical factors such as trauma, radiation and temperature, irritant and corrosive chemical substances, as well as tissue necrosis and hypersensitivity reactions. It is the most primitive protective response of the body to noxious stimulation and also a common pathophysiology of many different diseases (Yu, 2012). It is characterized by the following clinical signs of inflammation: redness, heat, swelling, pain and dysfunction of the organs involved (Stankov, 2012). The can also act to lessen the activation threshold of nociceptors so that the stimulation needed to cause activation is

The purpose of the immune system is to prevent and minimize infections; this is how the body protects us from microbes that would otherwise make us ill or kill us (Dugdale, 2013). The immune system works by differentiating between our own cells (self-antigens), foreign cells (antigens), and pathogenic microbes (Dugdale, 2013). When our cells discover anything unfamiliar, our immune system works to destroy it(Dug dale, 2013). If the immune system cannot activate to kill foreign cells, we can get infections (Dugdale, 2013). Conversely, if it is activated without any foreign cells present it can cause pathopysiological problems (Dugdale,2013). This paper will focus on the

IRF-1 has antiviral, immunomodulatory, apoptotic, and immune cell differentiation effects. Experiments in IRF-1 knockout mice have demonstrated that IRF-1 is a key regulator of macrophage function, NK cell response, Th1/Th2 differentiation, and DC differentiation (94-97). IRF-1 is involved in the regulation of many genes during inflammation, immune responses, and cell proliferation. IRF-1 interacts with both IRF-2 and IRF-8 as an antagonist. IRF-2 is an antagonist that represses IRF-1 function by competing for IRF-1 binding sites, and IRF-8 inhibits IRF-1 function by directly binding to it (98, 99). IRF-7 is considered the “master” regulator of type I IFN signalling due to its role in providing the second stronger wave of type 1 IFNs. Honda et al. showed that in mice deficient in the IRF-7 gene that IRF-7 is required for the initiation of IFN-α/β genes by the MyD88-dependent pathway and the MyD88-independent pathway (10). It has been reported that IRF-7 is expressed at low levels in most cell types (78). The low levels of IRF-7 expression suggest that IRF-3 is mainly responsible for the initial induction of IFN, where IRF-7 is responsible for the later up regulation (78). This suggests a positive feedback loop where IRF-7 induced IFN expression is involved in the second and larger IFN induction step, which allows for efficient upregulation of type I IFNs during viral infection (78, 100, 101). IRF-7 expression is tightly regulated to prevent excessive tissue