Summary Veterinary Immunology

ISBN-10 1455703621 ISBN-13 9781455703623
416 Flashcards & Notes
6 Students
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This is the summary of the book "Veterinary Immunology". The author(s) of the book is/are Ian Tizard. The ISBN of the book is 9781455703623 or 1455703621. This summary is written by students who study efficient with the Study Tool of Study Smart With Chris.

Summary - 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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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