Human Immune System
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Antigens are molecules capable of stimulating an immune response. Each antigen has distinct surface features, or epitopes, resulting in specific responses.
Antibodies (immunoglobins) are Y-shaped proteins produced by B cells of the immune system in response to exposure to antigens. Each antibody contains a paratope which recognizes a specific epitope on an antigen, acting like a lock and key binding mechanism. This binding helps to eliminate antigens from the body, either by direct neutralization or by ‘tagging’ for other arms of the immune system.
Antibodies (immunoglobins) are Y-shaped proteins produced by B cells of the immune system in response to exposure to antigens. Each antibody contains a paratope which recognizes a specific epitope on an antigen, acting like a lock and key binding mechanism. This binding helps to eliminate antigens from the body, either by direct neutralization or by ‘tagging’ for other arms of the immune system.
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Measuring ER stress and the unfolded protein response using mammalian tissue culture system Christine M. Oslowski and Fumihiko Urano
Methods Enzymol. Author manuscript; available in PMC 2013 Jul 4., Published in final edited form as: Methods Enzymol. 2011; 490: 71–92.
AbstractThe endoplasmic reticulum (ER) functions to properly fold and process secreted and transmembrane proteins. Environmental and genetic factors that disrupt ER function cause an accumulation of misfolded and unfolded proteins in the ER lumen, a condition termed ER stress. ER stress activates a signaling network called the Unfolded Protein Response (UPR) to alleviate this stress and restore ER homeostasis, promoting cell survival and adaptation. However, under unresolvable ER stress conditions, the UPR promotes apoptosis. Here we discuss the current methods to measure ER stress levels, UPR activation, and subsequent pathways in mammalian cells. These methods will assist us in understanding the UPR and its contribution to ER stress related-disorders such as diabetes and neurodegeneration.
In order to create a tumor necrosis factor (TNF) knockout, an exon containing the nucleotides 3704–5364 was removed from the gene. This exon encodes a portion of the mature TNF domain, as well as the leader sequence, which is a highly conserved region necessary for proper intracellular processing. TNF-/- mice develop normally and have no gross structural or morphological abnormalities. However, upon immunization with SRBC (sheep red blood cells), these mice demonstrated a deficiency in the maturation of an antibody response; they were able to generate normal levels of IgM, but could not develop specific IgG levels.
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The tumor-suppressor protein p53 accumulates when DNA is damaged due to a chain of biochemical factors. Part of this pathway includes alpha-interferon and beta-interferon, which induce transcription of the p53 gene, resulting in the increase of p53 protein level and enhancement of cancer cell-apoptosis.[79] p53 prevents the cell from replicating by stopping the cell cycle at G1, or interphase, to give the cell time to repair, however it will induce apoptosis if damage is extensive and repair efforts fail.[80] Any disruption to the regulation of the p53 or interferon genes will result in impaired apoptosis and the possible formation of tumors.
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Spina Bbifida, the persistence of Interdigital Webs, and Open Brain.
Apaf-1 is the protein that turns on caspase 9 by cleavage to begin the caspase cascade that leads to apoptosis. Since a -/- mutation in the APAF-1 gene is embryonic lethal, a gene trap strategy was used in order to generate an APAF-1 -/- mouse. This assay is used to disrupt gene function by creating an intragenic gene fusion. When an APAF-1 gene trap is introduced into cells, many morphological changes occur, such as spina bifida, the persistence of interdigital webs, and open brain. In addition, after embryonic day 12.5, the brain of the embryos showed several structural changes. APAF-1 cells are protected from apoptosis stimuli such as irradiation. A BAX-1 knock-out mouse exhibits normal forebrain formation and a decreased programmed cell death in some neuronal populations and in the spinal cord, leading to an increase in motor neurons.
Severe Brain Malformation, Cardiac Failure and thus Embryonic Lethality.
Caspase 9, 8 and 3 knock-out
The caspase proteins are integral parts of the apoptosis pathway, so it follows that knock-outs made have varying damaging results. A caspase 9 knock-out leads to a severe brain malformation. A caspase 8 knock-out leads to cardiac failure and thus embryonic lethality. However, with the use of cre-lox technology, a caspase 8 knock-out has been created that exhibits an increase in peripheral T cells, an impaired T cell response, and a defect in neural tube closure. These mice were found to be resistant to apoptosis mediated by CD95, TNFR, etc. but not resistant to apoptosis caused by UV irradiation, chemotherapeutic drugs, and other stimuli. Finally, a caspase 3 knock-out was characterized by ectopic cell masses in the brain and abnormal apoptotic features such as membrane blebbing or nuclear fragmentation. A remarkable feature of these KO mice is that they have a very restricted phenotype: Casp3, 9, APAF-1 KO mice have deformations of neural tissue and FADD and Casp 8 KO showed defective heart development, however, in both types of KO other organs developed normally and some cell types were still sensitive to apoptotic stimuli suggesting that unknown proapoptotic pathways exist.
Severe Brain Malformation, Cardiac Failure and thus Embryonic Lethality.
Caspase 9, 8 and 3 knock-out
The caspase proteins are integral parts of the apoptosis pathway, so it follows that knock-outs made have varying damaging results. A caspase 9 knock-out leads to a severe brain malformation. A caspase 8 knock-out leads to cardiac failure and thus embryonic lethality. However, with the use of cre-lox technology, a caspase 8 knock-out has been created that exhibits an increase in peripheral T cells, an impaired T cell response, and a defect in neural tube closure. These mice were found to be resistant to apoptosis mediated by CD95, TNFR, etc. but not resistant to apoptosis caused by UV irradiation, chemotherapeutic drugs, and other stimuli. Finally, a caspase 3 knock-out was characterized by ectopic cell masses in the brain and abnormal apoptotic features such as membrane blebbing or nuclear fragmentation. A remarkable feature of these KO mice is that they have a very restricted phenotype: Casp3, 9, APAF-1 KO mice have deformations of neural tissue and FADD and Casp 8 KO showed defective heart development, however, in both types of KO other organs developed normally and some cell types were still sensitive to apoptotic stimuli suggesting that unknown proapoptotic pathways exist.
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An Incredible but Simple Immune System
Why Horseshoe Crab Blood Is So Valuable
https://www.youtube.com/watch?v=oXVnuG3zO_0 Horseshoe Crabs have an innate immune system which attacks based on the identification of a general threat. The basis for a horseshoe crab's immune response are cells called granular amoebocytes. When bacteria come into contact with a horseshoe crab's blood they trigger an enzyme cascade mediated by these amoebocytes which causes the blood in the immediate area of the infection to clot into a gel. The gel surrounds and isolates the infection from the rest of the crab and the pathogens are neutralized. |
Hunting for bats: How these animals could help find a way out of the pandemic https://www.ctvnews.ca/w5/hunting-for-bats-how-these-animals-could-help-find-a-way-out-of-the-pandemic-1.5146555?fbclid=IwAR2ZNsbKm0-FQb6UnPRLwsjyaEjkpQnaL3U56tifnCcA6o00g6Z90gGNEX8 Faure has teamed up with virologists at McMaster to experimentally determine how such a tiny animal could be so powerful against a virus that kills humans so easily. |
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It turns out some bats can live with coronaviruses in their bodies without getting sick at all. Understanding why bats fare so differently when faced with viral invaders than humans could be a game changer in the fight against the pandemic that has already claimed more than a million lives worldwide.
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Immunization of Older Adults
Nations has shown that the percentage of elderly people worldwide has increased from 8% in 1950 to 10% in 2000; this trend is expected to continue, with 21% of the population being elderly by 2050 [1]. As the immune response in the elderly declines and the outcome of infection is often poor, prevention of infections becomes critically important [4]. Immunosenescence also affects the response to immunisation, as shown by the reduced efficacy of annual influenza vaccination in the elderly, with an efficacy of 17–53% in the elderly, compared with 70–90% in healthy adults [7].
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READ MORE:
Challenges for vaccination in the elderly Richard Aspinall, Giuseppe Del Giudice, Rita B Effros, Beatrix Grubeck-Loebenstein & Suryaprakash Sambhara Immunity & Ageing volume 4, Article number: 9 (2007) https://immunityageing.biomedcentral.com/articles/10.1186/1742-4933-4-9 |
Guillain-Barré syndrome
Guillain–Barré syndrome is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system. Typically both sides are involved and the initial symptoms are changes in sensation or pain often in the back along with muscle weakness, beginning in the feet and hands, often spreading to the arms and upper body.Wikipedia
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