The skin, cornea and respiratory mucosa, gastrointestinal and genitourinary tracts form a physical barrier that serves as the body’s first line of defense. Some of these barriers have active immune functions:
The immune system is “non-self” to distinguish in a position between “self” and, eliminating potentially harmful foreign molecules and cells from the body. also recognizes and destroys it abnormal cells the body’s own tissue. Any substance that can be recognized by the immune system is referred to as antigen (Ag). The skin, cornea and respiratory mucosa, gastrointestinal and genitourinary tracts form a physical barrier that serves as the body’s first line of defense. Some of these barriers have active immune functions: The outer skin keratinocytes z. B. secrete antimicrobial peptides (defensins) and tallow and sweat forming glands secrete microbe-inhibiting substances from (eg., Lactic acid, fatty acids). In the skin also various cells of the immune system (eg. As mast cells, intraepithelial lymphocytes, Ag-presenting Langerhans cells) find. The mucosa of the respiratory and gastrointestinal and genitourinary tracts containing antimicrobials such as lysozyme, lactoferrin and secretory IgA antibodies (SIgA). The breaching of the anatomical barriers can trigger two different immune responses: the innate and the acquired. Many molecular components (eg. As complement, cytokines, acute phase proteins) are involved in both innate and acquired immunity. Innate immunity innate (natural) immunity requires no prior exposure to an antigen (i. E. Immunologic memory) to be effective. So it can respond to an intruder immediately. It recognizes rather large area distributed antigen molecules as it is specific for an organism or a cell. The components include scavenger cells Natural killer (NK) cells Polys phagocytes (neutrophils in the blood and tissues, blood monocytes, macrophages in tissue) take intruding antigens and destroy them. An attack by phagocytes is enabled when antigens (Ags) with antibodies (Ak) are enveloped, are produced as part of the acquired immunity or when complement coat the Ags. Natural killer cells kill off virus-infected cells and some tumor cells. Polymorphonuclear leukocytes (neutrophils, eosinophils, basophils, mast cells) and mononuclear cells (monocytes, macrophages) liberate inflammatory mediators. Acquired immunity Acquired (adaptive) immunity requires prior exposure to an antigen and thus takes time to develop after the first encounter with a new invader. After that response is fast. The immune system remembers the last exposure and reacts Ag-specific. The components T-cells B-cells include Acquired immunity cell mediated: of certain T-cell responses derived Humoral Immunity: derived from B-cell responses (B-cells release soluble Ag-specific antibody-free) B cells and T-cells work together to destroy invaders. Antigen presenting cells (immune system components: antigen presenting cells) are necessary to deliver Ags to T cells. Immune response activation, regulation and recovery of the immune response are required for a successful immune defense. Activation of the immune system is activated when a foreign antigen is recognized by circulating Ak or cell surface receptors. These receptors can be highly specific (Ak on B-cells or T-cell receptors) Coarse specific (z. B. pattern recognition receptors like Toll-like, mannose and scavenger receptors on dendritic cells and others). Coarse specific receptors recognize general microbial pathogen-associated molecular patterns in ligands such as Gram-negative lipopolysaccharide, Gram-positive bacterial flagellin Peptidoglykene unmethylated cytosine-guanosine dinucleotide (CpG motifs) and viral double-stranded RNA. Activation also takes place when Ak-Ag and complement-microorganism complexes to surface receptors for the Fc region (Fc = crystallizable fragment) of IgG (Fc?R), and bind to C3b and iC3b. Once detected, an antigen, an Ag-Ab complex or a complement microorganism complex is phagocytosed. Most microorganisms are killed, after they have been phagocytized, but others inhibit the intracellular killing ability of phagocytes (z. B. mycobacteria, which were swallowed by a macrophage, inhibit the killing ability of the cell). Cytokines derived from T cells, esp. Interferon-? (IFN-?) that stimulate in such cases, the phagocytes to increased production of lytic enzymes and other mikrobenabtötender products and thereby increase the ability to destroy microorganisms or encapsulate. If an antigen not immediately engulfed and completely dismantled (an unusual occurrence), the acquired immune response into action. This response begins in spleen in circulating antigen Regional lymph nodes in tissue-Ag mucosa associated lymphatic tissues (eg. B. tonsils, adenoids, Peyer’s patches) for mucosal Ag dendritic Langerhans cells of the skin phagocytose, for example, the antigen and migrate to local lymph nodes , There, the expression of Ag-derived peptides with class II molecules of the major histocompatibility (MHC, major histocompatibility complex) takes place on the cell surface, which present peptides to CD4 T-helper cells (TH). After binding of the MHC complex to the peptic TH-cell, it receives various costimulatory signals, forms the receptors for the cytokine IL-2 and secretes various cytokines. Each subset TH cells secretes various combinations of substances, thus producing different immune responses (components of the immune system: T cells). Class II MHC molecules typically give peptides derived from extracellular (exogenous) antigens (z. B. many bacteria) derived from CD4-TH cells. In contrast, class I MHC molecules enter typically peptides derived from intracellular (endogenous) antigens (z. B. viruses) of CD8 cytotoxic T-cells. Thereafter, the activated cytotoxic T cell destroys the infected Zelle.Regulierung To the host body from excessive damage to preserve (z. B. Anaphylaxis, large area tissue destruction), the immune response must be controlled. By the secretion of immunosuppressive cytokines like IL-10 and transforming growth factor-? (TGF-?), or by a defective defined mechanism of cell contact, engage regulatory T-cells (the majority of which the Foxp3 transcriptional factor expressing) helping in the control one of the immune response. These regulatory cells help prevent autoimmune reactions and are also likely in reversing current reactions to exogenous Ag beteiligt.Rückbildung The immune response is completed when the antigen is sequestered, or is eliminated from the body. Without stimulation by antigen, cytokine secretion stops and activated cytotoxic T cells undergoing apoptosis. This marks the cells for immediate phagocytosis, whereby the release of the cell contents is prevented by formation of an inflammatory response. T and B cells that have differentiated into memory cells spared this fate. Geriatric Basics With age, the immune system becomes less effective in the following manner: The ability of the immune system to distinguish from Private alien, decreases so that autoimmune diseases are more common. Macrophages destroy bacteria, cancer cells and other Ag slower and may contribute to the increased incidence of cancer in the elderly. T cells respond less quickly to antigens. There are fewer lymphocytes, which can respond to new antigens. The aging body produces in response to bacterial infections less complements. Fewer antibodies in response to antigens produced and the antibodies are less to dock in a position to the antigens, possibly in older people contribute to the increased incidence of pneumonia, influenza, infectious endocarditis and tetanus, as well as the increased risk of death by this disease does. These changes may also partly explain why vaccines in the elderly are less effective.