Samenvatting Veterinary Immunology

ISBN-10 1455703621 ISBN-13 9781455703623
416 Flashcards en notities
6 Studenten
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Dit is de samenvatting van het boek "Veterinary Immunology". De auteur(s) van het boek is/zijn Ian Tizard. Het ISBN van dit boek is 9781455703623 of 1455703621. Deze samenvatting is geschreven door studenten die effectief studeren met de studietool van Study Smart With Chris.

Samenvatting - Veterinary Immunology

  • 1 The Defence of the body

  • History of immunology
    - Chinese were the first to realize that people who had infectious diseases were immune to later outbreaks
    - they started to infect people on purpose
  • Louis Pasteur
    - has found out that with old infectious bacteria animals became immune to the dangerous young form 
    - even dead parts of bacteria could do this
  • Commensals
    Microorganisms that do not invade or cause disease
  • Agressive micro-organisms
    - if they succeed in invading the body and overcoming the immune defenses they can cause disease 
    -> they are called pathogens
  • Virulence
    The ability to cause disease
  • Primary pathogens
    - can cause disease in low numbers
  • Opportunistic pathogens
    Cause disease when the immune defense is weakened or when they are with many
  • Physical barriers
    - the first line of defense against pathogens is the skin
    - coughing
    - sneezing
    - vomiting
    - diarrhea
    - secreting mucus
  • Innate immunity
    - activated immediately when a pathogen enters where it should not -> inflammation
    - sentinel cells -> can detect molecules associated with invading microorganisms -> recruit (werven) leukocytes  
    - lacks any form or memory
  • Adaptive immunity
    - recognize and destroy invaders 
    - learn from the process
    - the more often it encounters a specific pathogen -> the more effective the destruction
    - it does develop quite slowly
  • Difference between adaptive and innate
    - in the way they recognize pathogens
    - innate system -> binds molecules commonly expressed on many different microbes
    - adaptive system -> generates a lot of completely new receptors  that can bind a wild array of foreign moleculs 
    - bacteria and viruses require different systems because one originates outside the body and the other inside the body's own cells.
  • Exogenous invaders
    - external invaders
    - humoral immune respons 
    - antibodies are used to promote destruction of these invaders.
  • Endogenous invaders
    - intracellular
    - cell-mediated respons 
    - uses specialized cells
  • Antibodies
    - the protective molecules found in serum of immune animals
    - binds to antigens
    - can be generated quicker if they have been generated before
  • Antigens
    -Foreign substance 
    - is trapped, processed, and prestented by several dell types (dentritic cells and macrophages)
  • Anamnestic repsons
    The second respons to one pathogen
  • B/T-lymphocytes
    - have receptors for foreign antigen, can bind to them and respons appropriately
    - function as memory cells
  • T-lymphocytes
    - cell-mediated respons
    -> t-helper cells : promote immune respons
    -> T regulatory cells : inhibit immune response
  • B-lymphocytes
    Mediate anti body-mediated respons
  • 2 Innate Immunity: The Recognition of Invaders

  • Innate system
    - destroying bacteria fast
    - has developed in animals as well as plants
    - causes inflammation
  • Inflammation
    - makes leukocytes and antimicrobial molecules gather at sites of invasion. 
  • Exogenous signals
    - invading microorganisms
    - consists of molecules produces by microbial invaders
    -these are called -> Pathogen-Associated Molecular Patterns (PAMP's)
  • Endogenous signals
    - dead and dying cells
    - consist of molecules released from damaged celles
    -> These are called -> Damage-Associated Patterns (DAMPs)
  • PRRs
    - Pattern Recognition Receptors 
    - recognize PAMPs and Damps and activates the immune system 
    - most PPRs are cell-associated receptors found on cell membranes -> within the cytosol, within cytoplasmic vesicles
    - or solutes circulating the blood stream
  • Invading microorganisms
    - they have a wide variety of ever changing molecules on their surface
    - the body choses to use receptors that bind to abundant, essential molecules that are common to many microorganisms
  • TLRs
    - Toll-like receptors
    - located either on cell sufaces or within the cells
    - are part of the innate immune system
    - they can detect body invaders and cell invaders
    - they can be found on sentinel cells
    - transmembrane glycoprotein receptors
  • Sentinel cells
    - refer to cells in the bodyś first line of defense
    - macrophages, mast cells, dentritic cells and epithelial cells
  • Cascade TLRs
    - PAMP binds to a TLR multiprotein complex -> a signal tranduction starts -> proinflammatory molecules
    - cytokines -> different TLRs and different PAMPs -> different responses -> Example: Leukocyte
  • Cytokines
    - regulate activities of cells involved in the defense of the body
    - produces inactive and can be activated by the enzyme caspase-1
  • Inflammasome
    - production of caspases -> initation of inflammation
  • IFNs
    -type I interferons (antiviral cytokines)
    - viral invaders trigger the synthesis of IFNs
    - proteins that activate genes encoding for antiviral proteins
  • RIG-1-like receptors
    - retinoic acid inducible gene-like receptors (RLRs) 
    - expressed in the cytosol 
    - recognize viral dsRNA
    - triggered -> activate caspases -> production of type 1 IFNs
  • NOD-like receptors
    - nucleotide-binding oligomerization domain-like receptors (NLRs) 
    - can detect pathogens in the cytosol
    - binding activates the production of proinflammatory cytokines 
    - or the production of the antimicrobial proteins -> defensins
  • C-type lectin receptors
    - proteins that bind carbohydrates in a calcium dependent manner
    - many different types of lectins
    - some are cell surface PRRs
  • Bacterial lipopolysaccharides
    - LPS
    - do not bind to TLR4 directly 
    - only bind if they have been linked to the three other proteins
    - LPS binds to LPS-binding protein -> this binds to a complex called CD14/TLR4/MD-2 -> triggers cytokine production and activates macrophages
  • Bacterial peptidoglycans
    - found in the cell walls of Gram-positive and -negative bacteria. 
    - peptidoglycan recognition proteins (PGRPs) are PRRs that induce the production of proinflammatory and antimicrobial peptides
  • Bacterial DNA
    - structurally different from that of eukaryotes
    - it can be recognized
    - parts can bind to TLR9 -> triggers production of cytokines
    - rich in unmethylated CpG
  • Virus
    - usually consists of a nucleic acid core, surrounded by a layer of protein (capsid) and possibly a lipid envelope  
    - the nucleic acids are different than those in animals and can be recognized.
    - Intracellular RLRs detect and repsond to viral dsRNA
  • DAMPs
    - are released when cells die (intracellular) or when tissues get damaged (extracellular)
    - some intracellular DAMPs are released by the mitochrondia
  • HMGB1
    - high mobility group box protein-1
    - normally binds DNA and ensures folding is done correctly
    - triggers inflammation
    - secreted by activated macrophages -> escapes from broken cells
    - sustains and prolongs inflammation
    - stimulates the growth of new blood vessels
  • Heparan sulfate
    - An important extracellular DAMP
    - normally found in cell membranes and the extracellular matrix
    - membranes of matrix is damaged -> the heparin gets loose -> enters into tissue fluids -> acts as a DAMP
  • Pentraxins
    - P-type lectins
    - formed by 5 proteins
    - function is to activate, complement and stimulate leukocytes
  • Galectins
    - S-type lectins
    - play a role in inflammation by binding leukocytes to the extracellular matrix
  • Collectins
    - C-type lectins
    - very large family of proteins with many different roles
    - require calcium to bind to carbohydrates
    - C-terminal binds to carbohydrates
    - N-terminal interacts with cells or complement components
    - especially important in very young animals
    - produced by the lungs and the liver
  • MLB
    - mannose-binding lectin
    - the most important one
    - it binds very strongly to bacteria and to yeast
    - can also bind viruses as well as parasites 
    - bacteria bound to MLB are ingested by phagocytic cells
  • Sentinel cells
    - primary function is to recognize and respond to invading microbes
  • Macrophages
    - The most important sentinel cells
    - can capture, kill and destroy microbial invaders
  • Dendritic cells
    - possess long, thin cytoplasmatic processes -> dendrites
    - closely related to macrophages
  • Mast cells
    - play a key role in allergies
    - can trigger inflammation
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Laatst toegevoegde flashcards

Welke reactie is niet cel-gemedieerd?
- serumziekte
IgA kan door het lichaam in de darmlumen worden uitgescheiden
- IgA kan binden aan de poly-lg receptor op mucosale epitheel cellen
De MHC-basis voor genetische effecten op de immuunrespons leidit tot de volgende stellingen
- alle antwoorden zijn juist
IL-2 niet correct
- Il-2 bindt antigeen middels een Fab fragment
Bindt aan een niet-variabel deel van MHC klasse I moleculen
Een t helper 2 respons wordt gekenmerkt door
- een verhoogde interleukine-4 productie
De term celgebonden of cellulaire immuniteit slaat op het feit dat>
- De immuniteit het resultaat is van de productie van antilichamen door T-cellen
Een antilichaam Fc fragment bevat
- complement binding regio's
Een antilichaam Fab fragment bevat:
- Complementary determining regions (CDR regio's)
3 beweringen -> juist?
- Alleen bewering 2 is juist
- De aviditeit van IgM is doogaans hoger dan die van IgG