Introduction Flashcards
Immunity
Actively resist disease
Immunology
Study of immunity
Immune system
Network of cells, tissues, organs, and the substances they make that helps the body fight infections and other diseases
Physical barrier
Chemical barriers
Adaptive immune system summary
Innate response
Innate immunity
Relies on recognition of pathogen-associated molecular patterns (PAMPs) by pathogen recognition receptors (PRRs)
PAMPs
Pathogen-associated molecular patterns
-small, conserved, molecular motifs
PRR classes
- Toll-like receptors
- RIG-like receptors
- Nod-like receptors
- C-type lectin receptors
Phagocytosis and oxygen dependant killing
-Induce production of reactive oxygen species (ROS)
-Catalyse oxidation of microbial constituents= microbial killing
-Happens within the phagolysosome
Inflammatory response
Antigen presentation
-T cell receptors (TCRs) recognise antigens
-Antigens are presented to T cells via major histocompatibility complex (MHC) proteins
Macrophae interaction with S.aureus
Classes of T cells
- Cytotoxic (Tc): releases performing and granzyme (cell lysis)
- Helper (Th): releases cytokine (inflammation)
Opsonization
Immune process which uses opsonins, eg antibodies, to coat pathogens and other particles, making them easier for phagocytes to eat
Antibody production
Complement system
Proteins that are recruited by bound Abs to:
1. Directly lyse cells
2. Induce opsonization
Antibody mediated response
Primary and secondary antibody response
Immunogen
substance that induces an immune response
Epitope
Portion of anigen bound by the antibody/TCR
- 4-6 aa
- Antibodies bind nativ epitopes
- TCR bind digested/linear epitopes
TCR structure
-Membrane spanning
-alpha chain and a Beta chain
-Variable domain: binds the antigen
-Constant domain
MHC1
-Major histocompatibility complex
-On all nucleated cells
- alpha chain encoded by MHC gene region
-Alpha chain embedded in membrane
- Beta chain encoded by non-MHC Beta-2-microglubulin (B2m)
MHC II
-On Beta cells, macrophages and dendritic cells (APCs)
-Alpha and Beta chain noncovalently linked and embedded in membrane
Cytotoxic T cells
-CD8+ cells
-Contact induce degranulation
-Perforin form pores in target cell
-Granzymes enter cell and induce programmed cell death
Natural killer cell mechanism
Three features of adaptive immune response
-specificity
-Memory
-Tolerance
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Myeloid precursor
Lymphoid precursor
Lymphoid precursor
Innate immune system
Physical
Chemical
Inflammatory response cells (innate response)
M1 Macrophage
Proinflammatory
-Microbial and tumoral
-Tissue damage
M2 macrophage
-Anti-inflammatory activity
-Phagocytosis
-Tissue regeneration and repair
-Angiogenesis and immunomodulation
-Tumor formation and progression
Specificty
Immune cells recognise and react with individual molecules via direct molecular interactions
Memory
The immune response to a specific antigen is faster and stronger upon subsequent exposure because the initial antigen exposure induced growth and division of antigen-reactive cell, resulting in multiple copies of antigen -reactive cells
Tolerance
Immune cells are not able to react with self antigens. Self-reactive cells are destroyed during the development of the immune response
IgG
Major circulating antibodies with 4 subclasses
-found in:
*Extracellular fluid
*blood and lymph
*crosses placenta
IgM
First antibody to appear after immunisation
-Strong complement activator
-Found in: blood and lymph, monomer is B cell surface receptor
IgA
Important circulating antibody and major secretory antibody
Found in:
Secretions (saliva, blood fluids)
Monomer in blood and dimer in secretions
IgD
Minor circulating antibody
Found in b lymphocyte surfaces
IgE
Involved in allergic reactions and parasitic immunity
found in:
Blood and lymph, Ch4 binds to mast cells ad eosinophils
Humural response
B cells binds to antigen
-The B cells ingest the antibody and present it on their surface of MHC class II
-The antigen binds to to the TCR on helper T cell
-This activates the B cell which causes clonal expansion to occur
-This causes the b cell to divide rapidly and differentiate into 2 types
-Plasma cells produce antibodies that can bind to the antigen
-Memory B cells provide long lasting immunity
inflammatory response
-Tissue damage and M infection is recognised by immune cells like macrophages
-These cells release chemokines and cytokines
-This causes inflammation as well as causes more immune cells to go to site of infection
inflammation main goals
-Destroy invading M
-Induce local blood clotting to reduce spread of infection
-repair injured tissue
Phagocytosis
-Recognition and adherance (PAMP binds to TLR)
-Engulfment (Phagosome)
-Fusion of phagosome with lysosome
Cell mediated response
-Infected cell presents antigens through its MHC molecules
-These become antigen presenting cells (APC)
-Cytotoxic (CD8+) T cells recognise abnormal cells through MHC class I and destroy them
-Helper (CD4+) T cells recognise MHC class II and activate other immune cells like macrophages and beta cells as well as cytokines
-Clonal expansion: Activated Cytoxic T cells from cytokines divide and differentiate into effector T cytotoxic cells (active T killer cell) and memory T cells
-effector cytotoxic cells then release enzymes like perforins and granzymes which induce apoptosis
TLR1/2
Ligand: Triacyl lipoproteins (Gram-positive bacteria)
Pathway: MyD88-dependent
Activates: NF-κB (Cytokines)
TLR2/6
Ligand: Diacyl lipoproteins (Gram-positive bacteria)
Pathway: MyD88-dependent
Activates: NF-κB (Cytokines)
TLR4
Ligand: LPS (Gram-negative bacteria)
Pathway: MyD88-dependent (Cytokines) & TRIF-dependent (Interferons)
Activates: NF-κB (Cytokines), IRF3 (Interferons)
TLR3
Ligand: Double-stranded RNA (Viruses)
Pathway: TRIF-dependent
Activates: IRF3 (Interferons)
TLR5
Ligand: Flagellin (Bacteria)
Pathway: MyD88-dependent
Activates: NF-κB (Cytokines)
TLR7/8
Ligand: Single-stranded RNA (Viruses)
Pathway: MyD88-dependent
Activates: NF-κB (Cytokines), IRF7 (Interferons)
TLR9
Ligand: CpG DNA (Bacteria and viruses)
Pathway: MyD88-dependent
Activates: NF-κB (Cytokines), IRF7 (Interferons)
