Basic Immunity

Intrinsic immunity is also sometimes referred to as antiviral immunity it refers to a type of innate immunity that restricts viral replication and assembly. In addition to your innate and adaptive immunity, science shows that organisms have evolved to express genes that can prevent or suppress viral infections. These genes specifically target eukaryotic retroviruses. (Eukaryote, any cell or organism that possesses a clearly defined nucleus). Innate and adaptive immunity is activated after pathogen infection, intrinsic immunity factors were discovered with APOBEC3G, TRIM5a, Tetherin, and SAMHD1. This family of proteins has been suggested to play an important role in innate antiviral immunity. Those factors were discovered when researchers studying the viral replication of HIV-1 found that Tetherin and APOBEC3G could inhibit a wide range of viral species. Research also shows that many cells express intrinsic factors and can limit the replication of other non-retroviral species. When host cells are invaded by viruses, they can deploy multifaceted intracellular defence mechanisms to control infections and limit the damage they may cause. Host intracellular antiviral immunity can be classified into two main branches of an immune response - intrinsic immunity and interferon independent antiviral response.

The words intrinsic and innate have been used interchangeably within virology for a while now but they do not confer the same immune response. Apolipoprotein B Editing Complex (APOBEC3) is a family of cytidine deaminases that play important roles in intrinsic responses to infections by retroviruses. This family has been implicated in the control of other viruses such as herpes virus, human papillomavirus, hepatitis B virus, and parvovirus. APOBEC3 Proteins have been found to inhibit replication of HIV-1 that lacks the viral infectivity factor “Vif.” The viral infectivity factor is a protein found in HIV and its role is to disrupt the antiviral activity of the human enzyme APOBEC. VIF can bind APOBEC3D, APOBEC3F, and APOBEC3H in the apolipoprotein editing family, and target them for ubiquitination and degrade them in the proteasome. When these proteins are not disrupted, they can inhibit infection by eliminating the deoxycytidine residues that would induce mutations in newly synthesized HIV-1 coding strand DNA. AOPBEC3 Proteins can be expressed in different levels in hematopoietic cell populations including CD4+. And CD8+

Tetherin was discovered through the characterization of HIV-1 accessory protein Vpu. Vpu can enhance the release of HIV in other retroviral virions, which promotes replication. Tetherin was later identified through comparative microarray analysis. It is thought to hold virions at the cell surface by inserting the GPI membrane anchor into the viral envelope. Tethered Virions can then be internalized by endocytosis and degraded by endosomes. Tetherin also targets other enveloped viruses such as retroviruses (MLV, HTLV-1), filoviruses (Ebola virus), and herpesvirus (KSHV). SAMHD1 is a cellular enzyme responsible for blocking the replication of HIV in dendritic cells, macrophages, monocytes, and CD4+ T lymphocytes. SAMHD1 inhibits HIV-1 reverse transcription in the immune responses to HIV. SAMHD1 is the only mammalian protein that contains a SAM domain that is predicted to mediate protein-protein interaction. SAMHD1 plays a role in limiting innate immune signaling to HIV replication. TREX1 Has also been shown to be important for HIV replication, specifically innate immune responses to HIV DNA. These cellular enzymes are associated with the same autoimmune disease they can exhibit opposite effects on HIV-1 replication. SAMHD1 is antiviral whereas TREX1 is proviral for HIV-1 through very distinct mechanisms both proteins appear to target the reverse transcription step in HIV infection

Innate immunity refers to nonspecific defense mechanisms that are activated within minutes to hours after infection, this type of immunity involves the physical barriers of the skin. It can become an adaptive response if the infection reaches a dangerous threshold. Innate immunity refers to cellular receptors that recognize Pathogen-Associated Molecular patterns (PAMPs) and then activate signaling pathways leading to the production of interferons. This type of immunity leads to the expression of a large number of Interferon-stimulated Genes (ISGs) in both the infected cell and uninfected cells. PAMPs Can activate innate immune responses and protect the host from infection by identifying some conserved non-self-molecules. Bacterial lipopolysaccharides, endotoxins found on the cell membranes of gram-negative bacteria are considered to be a type of pathogen-associated molecular pattern. PAMPs Are recognized by toll-like receptors and pattern recognition receptors. In most situations, these molecules displayed on injured or infected transformed human cells are recognized as a part of innate immunity but they are often referred to as dangerous associated molecular patterns (DAMPs) instead of pathogen-associated molecular patterns. DAMPs can also include heat shock proteins. The body can make use of both PAMPs, and DAMPs. DAMPs Are endogenous molecules that are released from dying cells that play a role in innate immune activation. Even though these dangerous associated molecules can contribute to the host defense they can also promote a chronic inflammatory response as they react.

Adaptive immunity refers to the selection and rapid expansion of T cell and B cell clones. This type of immunity refers to antigen-specific immune responses. This immune response is more complex than the innate. An antigen must be processed and recognized. Once the antigen is recognized the adaptive immune system creates a specific army of immune cells that are designed to attack the antigen specifically. Adaptive immunity also includes antigen memory which means that future responses to the same antigenic threat is a bit more effective. The function of adaptive immune response is to destroy any invading pathogen or toxic molecules the response to pathogens is destructive so it must be only made in response to the molecules that are formed to the host and not the host itself. A fundamental feature of adaptive immunity is the ability to distinguish what is formed and what itself sometimes this mechanism can fail with its distinction and react destructively against the host on molecules which creates an autoimmune disease. Any substance that is capable of eliciting an adaptive immune response is referred to as an antigen. Adaptive immune responses are carried out by lymphocytes which are white blood cells and there 2 different response types--Antibody response and cell-mediated immune responses that are carried out by different classes of lymphocytes known as B cells and T cells. In an antibody response, the B cells are activated to secrete antibodies which are proteins known as immunoglobulins. In the cell-mediated response, The T cells are activated to react directly against a foreign antigen that is on the surface of a host cell. In cell-mediated immunity, The T cells might kill a virus-infected wholesale that has viral antigens on its surface to eliminate the infected cell before the virus has a chance to replicate and affect other cells.

How all three subsets work Synergistically

Adaptive and innate immunity are the well-known subsets of the immune system. Intrinsic immunity combines the aspect of both traditional branches, but it is very distinct. The innate immune system is typically the first to respond to pathogens and does not retain a memory of previous responses. This immunity is older than adaptive immunity. While innate immunity recognizes viral infections using toll receptors or pattern recognition receptors, intrinsic immunity is specific in both virus recognition and their mechanism of viral attenuation. Adaptive immunity is specifically tailored to a single class of pathogens like intrinsic immunity. Adaptive immunity must sense the infection to be turned on, intrinsic immunity proteins are constitutively expressed in ready to shut down the infection immediately following viral entry. The immune system works beyond the cellular and molecular level through an intricate system of tissues and organs that collaborate to protect the body from harmful cells in the fight against diseases. Many of the immune tissues and organs include the appendix, bone marrow, lymph nodes, the skin, the thymus gland, in the spleen.

The immune system functions through the actions of many cells and proteins. The core cells are Macrophages which can be triggered to recognize antigens such as damaged cells or for material or far on demand destruction. Macrophages are present in most tissues and only respond when they are needed for infections and dying cells. The primary mechanism of action that macrophages present is to take up various pathogenic threats to destroy them through phagocytosis, which is the eating in the degradation of the pathogen. Myeloid cells can give rise to many types of other immune cells including dendritic cells and macrophages. Natural killer cells (NK cells) are derived from the lymphoid lineages. They are similar to B cells. They develop in the bone marrow and have no antigen-specific receptors. Natural killer cells contain inhibitory cell surface receptors that recognize molecules that are a threat. Natural killer cells only kill cells that have downregulated class of human leukocyte antigen expression. The natural killer cells serve an important purpose for targeting virally infected cells in tumor cells. The NK cells are a subtype of T cells that can express certain receptors and markers.

B cells Are typically the critical cells in the blood that can mediate antibody production. When the host is presented with harmful material that harmful material is recognized as an antigen by a specific receptor on the B cells and after the B cells processed the antigen with the help of the T cells, the B cells can mature into plasma cells that secrete antibodies. One of the most unique features of The B cells is their ability to undergo isotope switching. T cells play a critical role in cell-mediated immunity, T cells also arise from the lymphoid linage and once a lymphoid progenitor cell commits to becoming AT cell it will then migrate to the bone marrow to the thymus, which is where it gets its name ("T" cell). The time is providing a suitable environment where T cells can develop into various subtypes. T cells can be induced to become T helper cells once they arrive in the blood or peripheral tissue. A B-Cell can Show an antigen to the T cell and if its receptor has an affinity the T cell was recognized the antigen.

T cells can activate a series of internal pathways that allow for antigen recognition to be verified. Once T helper cells have recognized their antigen, they can release a variety of cytokines which are molecules that signal to other immune cells and teach them how to appropriately respond to harmful molecules. There are several subsets of T helper cells including TH 1, TH2, and TH17. Dendritic cells are also part of the immune system and are similar to macrophages. Dendritic cells can engulf cellular informed material but instead of digesting it for removal the dendritic cell can process the material and present it as antigens to the T cells. Dendritic cells serve as antigen-presenting cells or accessory cells therefore, they relate information about pathogens between the innate and adaptive immune systems.

A well-functioning immune system is key to providing a good defense against most pathogenic organisms and to provide tolerance and resilience to non-threatening organisms. The immune system works by providing an exclusion barrier, identifying or eliminating pathogens, and identifying and tolerating non-threatening sources of antigens and maintaining a memory of immunological encounters. Practically all forms of immunity are affected by protein-energy malnutrition because most cells and enzymes are proteins that are made up of amino acids. Many of the biochemical pathways in the body that are used when the immune system is activated require vitamins and minerals as cofactors there is not one biochemical pathway that does not require a vitamin or a mineral as a cofactor to run its pathway. It is seen in many scientific articles how a deficiency in one small mineral per se zinc can cause a multitude of immune errors.

Nutrient status is an important factor contributing to immune competence. Undernutrition impairs the immune system, suppressing immune functions that are fundamental to host protection. Nutrients have been demonstrated to be required for the immune system to function efficiently these include essential amino acids, essential fatty acids, fat-soluble in water-soluble vitamins, micro and macronutrients. Practically all forms of immunity can be affected by deficiencies in one or more of these nutrients. The immune system is very dependent on micro and macronutrients is dependent on adequate hours of sleep, and physical movement. Physical activity and nutrition are vitally imperative for immune competency. An insufficient amount of physical activity has been classified by the World Health Organization as a leading risk factor for global mortality from non-communicable diseases. Engaging in an appropriate amount of regular physical activity is associated with reductions in all-cause mortality. Hey, poor diet is also associated with negative health consequences. Studies have shown that regular exercise can contribute to the reduction or delaying of onset immunosenescence. Researchers found that exercise can increase the output of T lymphocytes from the thymus. In the regularion of nutrition in physical exercise and sleep, there's a lot of research on how antioxidants can play a beneficial role in immunity competence and they can even go as far as preventing many well-known diseases.


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