Immune System
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+ | == Innate Immunity == | ||
+ | The blood plasma consists of Albumins and Globulines (IgG,IgA,IgM,IgD,IgE). The latter are antibodies which together with proteins of the '''Complement System''' also found in the blood are involved in the immediate immune response to invaders. | ||
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+ | The so called '''Sentinel Cells''' are located in our skin to detect invasions by e.g. microbes and viruses in terms of the ''innate'' immune response. ''Macrophages'' and ''dendritic cells'' as well as ''mast cells'' belong to the class of antigen representing sentinel cells. When an infection is caused by invaders entering our tissue through a damaged epidermis (wound), the sentinel cells respond by releasing ''cytokines'' (there are about 50 different cytokines e.g. TNF and Interleukins [IL-1,IL-2, ... , IL-35]). Sentinel cells do not recognise molecules that allow them to classify specific cell types but rather broad classes of invaders such as for example viruses or bacterial cells by ''Pattern Recognition Receptors'' [e.g. TLR,CLR,NLR] (as opposed to the ''adaptive'' immune response that is more specific). | ||
+ | Cytokines cause vascular endothelial cells to produce ''adhesion molecules'' (E-selectin, P-selectin) and lead to ''vasodilation'' (widening of bood vessles). This results in [[extravasion]] of [[rolling leukocytes]] into the tissue and allows antibodies to enter the infection site. Chemokines presented by edothelial cells are specifically recognised by chemokine receptors of some leukocytes. Binding to the chemokine receptor activates extravasion, leukocytes bind to endothelial cells via ICAM-1/LFA-1 and then transmigrate into tissues. The recruited leukocytes then help to fight the infection. This process is known as inflammation and is accompanied by the cardianl signs: Dolor (pain), Calor (heat), Rubor (redness), Tumor (swelling), Functio laesa (loss of function). | ||
+ | The first leukocytes that fight infection are the [[neutrophiles]], they are able to chase and engulf invadors. They are short-lived and have to be constantly produced by hematopoietic stem cells in the bown marrow. For infections lasting longer than a day, differnent chemokines are prouced, that attract another class of leukocytes known as monocytes, they are also involved in wound healing. | ||
+ | == Adaptive Immunity == | ||
+ | The ''adaptive'' or ''specific'' immune response is triggered by dendritic cells that carry ''antigens'' (pathogen molecules) of the detected pathogen that are transported to a lymph node through lymphatic vessles. In the lymph node T-cells (also called T-lymphocytes) are activated by antigens presented by the dendritic cell. Activated T-cells mature into CD4 and CD8 cell types, each attacking the invader with a different strategy. | ||
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+ | CD8-T-lymphocytes recognise a special class of antigen presenting complexes called MHC-class I (major histocompatibility complex), whearas CD4-T-lymphocytes recognise MHC-class II antigen presenting complexes. | ||
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+ | ---- | ||
+ | see also | ||
+ | https://www.youtube.com/watch?v=mFNxXfwlP3A |
Latest revision as of 12:09, 19 November 2015
[edit] Innate Immunity
The blood plasma consists of Albumins and Globulines (IgG,IgA,IgM,IgD,IgE). The latter are antibodies which together with proteins of the Complement System also found in the blood are involved in the immediate immune response to invaders.
The so called Sentinel Cells are located in our skin to detect invasions by e.g. microbes and viruses in terms of the innate immune response. Macrophages and dendritic cells as well as mast cells belong to the class of antigen representing sentinel cells. When an infection is caused by invaders entering our tissue through a damaged epidermis (wound), the sentinel cells respond by releasing cytokines (there are about 50 different cytokines e.g. TNF and Interleukins [IL-1,IL-2, ... , IL-35]). Sentinel cells do not recognise molecules that allow them to classify specific cell types but rather broad classes of invaders such as for example viruses or bacterial cells by Pattern Recognition Receptors [e.g. TLR,CLR,NLR] (as opposed to the adaptive immune response that is more specific).
Cytokines cause vascular endothelial cells to produce adhesion molecules (E-selectin, P-selectin) and lead to vasodilation (widening of bood vessles). This results in extravasion of rolling leukocytes into the tissue and allows antibodies to enter the infection site. Chemokines presented by edothelial cells are specifically recognised by chemokine receptors of some leukocytes. Binding to the chemokine receptor activates extravasion, leukocytes bind to endothelial cells via ICAM-1/LFA-1 and then transmigrate into tissues. The recruited leukocytes then help to fight the infection. This process is known as inflammation and is accompanied by the cardianl signs: Dolor (pain), Calor (heat), Rubor (redness), Tumor (swelling), Functio laesa (loss of function).
The first leukocytes that fight infection are the neutrophiles, they are able to chase and engulf invadors. They are short-lived and have to be constantly produced by hematopoietic stem cells in the bown marrow. For infections lasting longer than a day, differnent chemokines are prouced, that attract another class of leukocytes known as monocytes, they are also involved in wound healing.
[edit] Adaptive Immunity
The adaptive or specific immune response is triggered by dendritic cells that carry antigens (pathogen molecules) of the detected pathogen that are transported to a lymph node through lymphatic vessles. In the lymph node T-cells (also called T-lymphocytes) are activated by antigens presented by the dendritic cell. Activated T-cells mature into CD4 and CD8 cell types, each attacking the invader with a different strategy.
CD8-T-lymphocytes recognise a special class of antigen presenting complexes called MHC-class I (major histocompatibility complex), whearas CD4-T-lymphocytes recognise MHC-class II antigen presenting complexes.