Exam
Immunity
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Immunity
, Immune System, Immune Status, Immunology, Innate Immunity, Adaptive Immunity
See Also
Humoral Immunity
(
Immunoglobulin
)
T-Lymphocyte
B-Lymphocyte
Antigen Processing
Complement Pathway
Immunodeficiency
Definitions
Innate Immunity (Natural Immunity)
Gene
ralized, immediate immune response not reliant on prior exposure
Adaptive Immunity
Organism specific Immunity that relies on prior "memory" of exposure
Phagocyte
(and
Phagosome
,
Phagocytosis
)
Immune cells (
Neutrophil
s and
Monocyte
s/
Macrophage
s) are
White Blood Cell
s that engulf pathogens and foreign material
Phagosome
s are the membrane engulfed pathogens
Often combined with lysis by lysozymes
Lysosome
(and lysozyme)
Lysozyme-containing vacuoles produced in cellular golgi apparatus, and fuse with
Phagosome
s, resulting in pathogen lysis
Opsonin
(and
Opsonization
)
Proteins (e.g.
Antibody
, complement,
C-Reactive Protein
) that bind a pathogen surface, targeting it for
Phagocytosis
Types
Innate Immunity (Natural Immunity)
Physical Barriers
Skin
Mucosa (e.g. respiratory and gastrointestinal tract)
Cilia (e.g. respiratory)
Secretion Contents
Lysozyme (e.g. in tears,
Saliva
and in
Neutrophil
s)
Enzymatically degrades cell walls
Acid destroys acid-labile organisms
Sweat
Lactic Acid
Stomach
Gastric Acid (Hydrochloric Acid)
Phagosome
s (
Phagocytosis
)
Phagocyte
s such as
Neutrophil
s (PMNs) and
Macrophage
s attract and engulf organisms (
Phagocytosis
)
Phagocyte
s attract organisms which in turn activate
Phagocytosis
Phagosome
s are later lysed via
Lysosome
s (as below)
Lysosome
s
Neutrophil
's and
Macrophage
's (
Phagocyte
s) golgi apparatus produce
Lysosome
s (vacuoles) that contain lysozyme
Lysosome
s fuse with
Phagosome
s to produce phagolysosomes, degrading the engulfed organisms
Lysosome
s may also release their contents extracellularly to lyse larger targets too large to engulf
Natural Killer Cell
s (
NK cell
s)
Lymphocyte
s providing protection against
Intracellular Bacteria
and viruses
NK cell
s bind
Major Histocompatibility Complex
1 (
MHC-1
)
MHC-1
is present on normal cells and it inactivates
NK cell
s
MHC-1
is NOT expressed by infected cells
NK activating receptor
Ligand
is expressed
NK cell
s bind infected cells and destroy them
NK cell
mechanisms of infected cell destruction
Cytoplasmic granules
Perforin
Gene
rates pores on cells targeted for destruction
Granzyme
Induces programmed cell death (apoptosis) on entry into
Target Cell
s
Cytokine
s
Interferon
-Gamma (IFN-g)
Activates
Macrophage
s for
Phagocytosis
Image: NKC Mediated Destruction of Infected Host Cells
Complement Pathway
Images
Activation
Classical Pathway (C1, C2, C3, C4)
C1 binds
Antigen
-
Antibody
complex
Alternate Pathway (Properdin, Factor B, Factor D, C3)
Activation via microbe cell surface
Lectin Pathway (Mannose Binding Lectin or MBL)
Mannose Binding Lectin (MBL) binds mannose on microbe surface
Mannose Binding Lectin Associated Proteases (MASP-1, MASP-2) are activated
Classical Pathway (above) is stimulated
Enzyme C3 Convertase (C3bBb or C4b2a) Formation
Enzyme C3 Convertase splits C3 into C3a and C3b
C3a stimulates inflammation (attracts
Neutrophil
s, histamine release)
C3b stimulates
Phagocytosis
, inflammation (as with C3) and lysis (see below)
Opsonization
Microbe coated with an
Opsonin
, an
Antibody
or complement (e.g. C3b)
Surf
ace
Opsonin
s target microbes for
Phagocytosis
Phagocytosis
Phagocyte
s such as
Neutrophil
s (PMNs) and
Macrophage
s attract and engulf targeted organisms
Inflammation (via C3a, C5a)
Chemoattraction of
Neutrophil
s
Anaphylatoxic activation of
Mast Cell
s and
Basophil
s to degranulate, releasing histamines and vasoactives
Inflammation occurs when histamine-induced capillary dilation results in fluid and protein release
Lysis
C3b splits C5 into C5a and C5b
Membrane attack complex or MAC (C5b, C6, C7, C8, C9) binds microbe surface
MAC promotes microbe lysis
Types
Adaptive Immunity
Humoral Immunity
(B-Cells and Antibodies)
Humoral Immunity
(i.e. antibodies) targets extracellular pathogens
B Cell
s
Derivation
Fetal
Liver
Bone Marrow
Pluripotent Stem Cells
Peripheral Migration to Secondary Lymphoid Tissue
Spleen
Lymph Nodes
Peyer's
Patch
es (
Small Bowel
)
Activation
Images
Recognition
Antigen
binds
B-Lymphocyte Surface Receptor
(BCR)
BCR binding activates
B-Lymphocyte
T-Cell
Independent
Antigen
(e.g. inert
Antigen
s) alone activate B-Cells
T-Cell
Dependent
Antigen
(e.g. microbes) require added stmulus (e.g. T Cells)
B-Cell Proliferation
Activated
Lymphocyte
s proliferate
B-Cell Differentiation
Plasma Cells (
Antibody
producing cells)
Survive for days to weeks producing antibodies, and without replicating
Memory Cells
Remain in
B-Lymphocyte
pool ready to respond to the same
Antigen
in future
Future
Antigen
response is known as secondary immune response
Antibodies
Images
Immunoglobulin
(Ig)
Immunoglobulin
s (or antibodies) are Y-Shaped glycoproteins generated by Plasma Cells
Immunoglobulin
stem (Fc) is composed of 2 identical heavy chains
Two
Immunoglobulin A
rms emanate from the stem
Each arm is composed of 2 heavy chains and 2 light chains
The end of each arm contains an
Antigen
binding site (Fab)
Immunoglobulin
s have 2 forms
Membrane bound
Immunoglobulin
s (on surface of B-Cell)
Secretory
Immunoglobulin
(unbound, free-floating)
Monomeric antibodies exist as single
Antibody
molecules (IgE or IgG)
Multimeric antibodies exist as multiple joined antibodies (IgA or IgM)
Connected with J Chains
Immunoglobulin G
(IgG and subclasses IgG1-4)
Monomer accounting for 75% of all
Antibody
, and has a serum half-life of 23 days
Responsible for long lasting Immunity (secondary immune response) and
Type 2 Hypersensitivity
Immunoglobulin A
(IgA and subclasses IgA1, IgA2)
Dimer (2
Antibody
molecules) when secretory Ig and accounts for 10-15% of all
Antibody
Serum half life of 6 days
Present in body secretions (e.g. tears,
Saliva
, milk) and responsible for mucosal Immunity
Immunoglobulin M
(IgM)
Pentam
er (5
Antibody
molecules) when secretory Ig
Responsible for early, primary
Antibody
response
Immunoglobulin E
(IgE)
Long stem (Fc) monomeric
Antibody
with serum half-life of only 2.5 days
Reacts to allergans (
Type 1 Hypersensitivity
) and
Parasitic Infection
s
Immunoglobulin
D (IgD)
Monomer with serum half life of 3 days
Membrane bound surface
Antibody
Cell-Mediated Immunity (
T-Cell
s)
Cellular Immunity (i.e. T Cells) target
Intracellular Pathogen
s (e.g. viruses and
Intracellular Bacteria
)
T-Cell
s
Derived in
Bone Marrow
Migrate to
Thymus
Maturation and Differentiation into two cell lines with different
T-Cell
Receptors (CD4 and CD8)
Release into peripheral circulation
T-Cell Surface Receptor
s
T-Cell
Receptors (TCR)
Bind the
Antigen
on the
Antigen
presenting cell
TCR Types
TCR-alpha-beta (TCRab+)
TCR gamma-delta (TCRgd+)
T-Cell
Co-Receptors
CD4 binds
MHC Class 2
- peptide/
Antigen
complex on surface of
Antigen
presenting cells (APC)
Only Dendritic Cells,
Macrophage
s, B-Cells (
B-Lymphocyte
) present
MHC Class 2
CD8 binds
MHC Class 1
- peptide/
Antigen
complex on surface of
Antigen
presenting cells (APC)
Any nucleated cell can present
MHC Class 1
T-Cell
Types
Effector Cells
T-Helper Cell
s (CD4+ Cells)
Releases
Interferon
Stimulates
Phagocytosis
by
Macrophage
s
Activates
Natural Killer Cell
s
Suppresses viral replication
Releases interleuken 2
Promotes
T-Cell
proliferation (esp. memory cells)
Promotes B-Cell proliferation (memory cells and plasma cells)
T-Cytotoxic Cell
s (CD8+ Cells)
Target and destroy tumor cells and virus-infected cells
Other Cells
Memory Cells
Apoptosis of some cells not otherwise differentiated
Naive
T-Cell Activation
T-Cell
Receptor (TCR) binds to
MHC-Antigen complex
on
Antigen
Presenting Cells
T-Cell
Surf
ace CD28 binds to B7
Ligand
on
Antigen
presenting cell
T-Cell
Surf
ace LFA-1 (
Lymphocyte
Function Associated
Antigen
) binds ICAM1 on
Antigen
presenting cells
Interleukin
-2 (IL2) produced by naive T Cells
Stimulate T Cell proliferation
Resources
Immune System (Wikipedia)
https://en.wikipedia.org/wiki/Immune_system
References
Mahmoudi (2014) Immunology Made Ridiculously Simple, MedMaster, Miami, FL
Guyton and Hall (2006) Medical Physiology, p. 419-50
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