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Immunology

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by

Emily Lehan

on 5 December 2014

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Transcript of Immunology

Immunology
Lymphoid Progenitor
Myeloid Progenitor
Macrophage
Eosinophil
Neutrophil
Basophil
Dendritic Cell
B Cell
T Cell
Killer T Cell
Helper T Cell
TH1
TH2
TH17
Treg
Plasma cell
NK Cell
Dendritic Cell
Extracellular Pathogen
MHC found on chromosome 6
MHC is polygenic and polymorphic
MHC I
MHC II
Innate Immunity
Intravesicular Pathogen
TNF
Peptidoglycan
LPS
Flagellin
TLRs
TLRs
ds RNA
ssRNA
CgPDNA
T-Cell Selection
IFN
IFN
type 1 Interferons
Watch out nearby cells, there is a virus!
inhibit viral protein synthesis
degrade viral DNA
inhibit viral gene expression
Pro-inflammatory cytokines
HELP!
E-selectin
IL-
IL-
Neutrophils
NO
ROS
Proteolytic Enzyme
TCR
one Ag binding site
2. Positive Selection
3. Negative Selection
1. V(D)J rearrangement
beta chain rearrangement occurs first (D to J, then V to DJ. plus constant region C)
alpha chain next (V and J, plus a constant region C)
TcR must bind weakly to MHC (CORTEX)
TcR must not bind to self antigen being displayed by dendritic cells and macrophages in the corticomedullary zone
B-Cell Selection
activated B-cells undergo rounds of mutation (somatic hypermutation, aka affinity maturation) to select for higher affinity clones in the germinal centre of a lymph node

Naive B cells express IgM and IgD.

isotype switching will change the isotype of the Ab. The constant region of the Ab is coded by the "C" region with the greek letter that matches its name. Ie, IgG has a C(gamma) constant region.
T-cell activation
3) cytokine signaling recognition (naive and memory T-cells)
1) MHC-peptide-TcR recognition
2) co-stimulation recognition (CD28 on T cell and B7 on the dendritic cell)
Are initially made in bone marrow, interact with stromal cells and the IL-7 receptor
Pro B Cell: Heavy Chain Rearrangement V(D)J
Pre B-Cell: the chain associates with a surrogate light chain and Ig which together form a pre-B-cell receptor (not yet able to recognize antigen)
Immature B-Cell: Light chain rearrangement (V-J) of first the kappa chain gets 2 tries, then the lamda chain gets 2 tries -> mature IgM -> expressed on cell surface
Negative Selection: if recognize self antigen, they are destroyed
Go to the lymph nodes!!!
V(D)J
V(J)
PART A
PART B
ADCC: can bind to the Fc of IgG which binds to antigen on infected cell then kill it
IgE
IgG
IgM
IgA
IgD
Main place to find me:
Major Activiy
Complement Activation
All Areas,
highest in small intestine
MOST
COMMON
found everywhere
IgG1 &3- CONS
IgG2 &4-neutralization
Complement Activation
Opsonization
Neutralization
Sensitization for Killing by NK
Sensitization of mast cells
neutralization
mucosa
sensitization of mast cells
epithelial layer, bound to mast cells
doesnt really do much, found in very small amounts
Activated by
Inhibited by
1
2a
3
2b
IFN-
IFN-
TGF-
TGF-
IFN-
IFN-
IFN-
TGF-
TGF-
When can a B cell act all on its own without the help of a Th cell?

1) Specific Ag like LPS can elicit a polyclonal response without MHC presentation (it can bind to CD14 and provide the required signal)
2) bacterial polysaccharides with repetitive structure called TI-2 polymers can trigger Ab response by cross-linking several receptors at once

B-cell activation
T-Cell independent activation
T-cell dependent activation
Ag binding to BCR leads to endocytosis
Ag is presented on MHC class II
Seeing the Ag, and the CD40 together, the T cell gets ACTIVATED
it secretes CYTOKINES which in turn activates the B cell
The activation of CD40 by the TH cell results in proliferation (aka CLONAL EXPANSION) and maturation of the B cell.
the activated B cell will migrate to a lymph node, where it will undergo AFFINITY MATURATION, and ISOTYPE SWITCHING
memory cells are B cells which remain in the circulation long after the Ag has been cleared from the system
Memory B Cell
Hypersensitivity Reactions
Type 1
Type 2
Type 3
Type 4
Reactant
Diseases
Mechanism
IgE
IgG
IgG
TH1
TH2
CTL
Graft Rejection
Chronic Asthma, Chronic Allergic Rhinitis
Contact Dermatitis, Tuberculin rxn
Allergy, Asthma, Anaphylxis
Drug Allergy
Serum Sickness, Lupus,
Arthus reaction

Soluble/Cell Associated Ag?
Complement

Ab-FCeR1 alpha
Mast cell activation
Complement
Phagocytes
Macrophage
IgE production

Cytotoxicity
Main
Function
Releases
Controlled
by
Kill virus infected cells
Activate
macrophages
and B cells
mostly viruses, some intracellular bacteria
mostly microbes in vesicles, some extracellular bacteria
activate B cells, Ig class switch
Helminth parasites
enhance neutrophil response
extracellular bacteria
suppress T-cell response
signal to be this cell
TNF
IFN-
TNF
Perforin
Granzymes
Granulysin
upregulate FasL for programmed cell death
Innate Barriers:
A natomic
P hysiologic
P hagocytic
I nflammatory
Complement System
Classical
Lectin
Alternate
C3 Convertase
C5 Convertase
b-9
Membrane Attack Complex
inflammation
opsonization
Ab bound to Ag
Microbial surface (absence of Ab)
lectin bound to mannose
neutrophils monocytes, mast cells
Meet: The Cytokines
TNF
like to start fires (inflammation)
then call for help (neutrophils)
generally made by macrophages
Mainly an inhibitory cytokine. made by macrophages and Th2 cells (often SELF inhibitory
IFN-
IL-12 is produced by macrophages and dendritic cells, and causes release of IFN gamma and differentiation of Th cells to become TH1
IL-2 is released by T cells, and is a major growth factor for T cells, and also promotes growth of B cells
2
IL-4 and IL-5 are produced by TH2 cells and macrophages (IL-4), and cause the immune response to shift toward a TH2 response, activating antibody response (B cells) and eosinophils
2
TGF-
TGF beta inhibits the proliferation of T cells and activation of macrophages
Anti- Imflammatory Cytokines of TH2 (Humoral) Response
Pro-inflammatory Cytokines of the cell base TH1 response
IFN-
Macrophage activation
complement binding and opsonization
TGF-
TH1
TH2
TH17
TH3
CTLA4- expressed after activation, in place of CD28, turns down the immune response
CORTEX
Cortico-medullary zone
VJ
VDJ
Full transcript