Beruflich Dokumente
Kultur Dokumente
Immunoglobulins
Classes of Antibodies
IgM
Table 21.3
Classes of Antibodies
IgD
IgG
Classes of Antibodies
IgE
Table 21.3
Antigen-binding
site
Heavy chain
variable region
Heavy chain
constant region
Light chain
variable region
Light chain
constant region
Disulfide bond
Hinge
region
Stem
region
(a)
Figure 21.14a
Antibody Structure
Antibody Structure
Antibody Diversity
Antibody Targets
Ab mechanisms:
Neutralization
Agglutination
Precipitation
Complement fixation
Adaptive defenses
Humoral immunity
Antigen
Antigen-antibody
complex
Antibody
Inactivates by
Neutralization
(masks dangerous
parts of bacterial
exotoxins; viruses)
Agglutination
(cell-bound antigens)
Enhances
Enhances
Phagocytosis
Complement
Leads to
Inflammation
Cell lysis
Chemotaxis
Histamine
release
Figure 21.15
Monoclonal Antibodies
Monoclonal Antibodies
Types:
Memory T cells
Adaptive defenses
Cellular immunity
Immature
lymphocyte
Red bone marrow
T cell
receptor
Class II MHC
protein
T cell
receptor
Maturation
CD4
cell
Thymus
Activation
APC
(dendritic cell)
Class I MHC
protein
CD8
cell
Activation
Memory
cells
CD4
APC
(dendritic cell)
CD8
Lymphoid
tissues and
organs
Helper T cells
(or regulatory T cells)
Effector
cells
Blood plasma
Cytotoxic T cells
Figure 21.16
Targets
Targets
Antigen Recognition
MHC Proteins
Endogenous antigen
self-protein or foreign
(viral or cancer) protein
Cisternae of
endoplasmic
reticulum (ER)
3 Endogenous
antigen peptide is
loaded onto class
I MHC protein.
4 Loaded MHC protein
migrates in vesicle to
the plasma membrane,
where it displays the
antigenic peptide.
Transport
protein
(ATPase)
Antigenic peptide
Extracellular fluid
(a) Endogenous antigens are processed and displayed on class I MHC of all cells.
Figure 21.17a
Cytoplasm of APC
1a
Class II MHC is
synthesized in ER.
Invariant chain
prevents class II
MHC from binding
to peptides in the ER.
2a
Cisternae of
endoplasmic
Phagosome
reticulum (ER)
1b Extracellular
antigen (bacterium)
is phagocytized.
Class II MHC
is exported
from ER in a
vesicle.
2b
Phagosome merges
with lysosome, forming
a phagolysosome;
antigen is degraded.
Extracellular
antigen
Extracellular fluid
Lysosome
Vesicle with
loaded MHC
migrates to the
plasma
membrane.
Antigenic peptide
Figure 21.17b
T Cell Activation
Antigen binding
2.
Co-stimulation
Antigen binding stimulates the T cell, but costimulation is required before proliferation can
occur
T cells
Adaptive defenses
Cellular immunity
1 Dendritic cell
Viral antigen
Dendritic
cell
T cell receptor
(TCR)
Clone
formation
Class lI MHC
protein
displaying
processed
viral antigen
CD4 protein
engulfs an
exogenous antigen,
processes it, and
displays its
fragments on class
II MHC protein.
2 Immunocompetent
Costimulation
also required
activated,
proliferate (clone),
and become memory
and effector cells.
Helper T
memory cell
Activated
helper
T cells
Figure 21.18
Cytokines p. 818
Cell development
Differentiation
Include:
Cytokines
Helper T Cells
Helper T cell
Class II MHC
protein
APC (dendritic cell)
1 Previously
activated TH cell
binds dendritic cell.
2 TH cell stimulates
IL-2
Class I
MHC protein
(b)
CD8
protein
CD8 T cell
Helper T Cells
Helper T cell
CD4 protein
self-nonself complexes of a
B cell that has encountered
its antigen and is displaying
it on MHC II on its surface.
MHC II protein
of B cell displaying
processed antigen
2 TH cell releases
interleukins as
co-stimulatory signals to
complete B cell activation.
Figure 21.19a
Targets
Virus-infected cells
Cancer cells
Cytotoxic T Cells
Cytotoxic T Cells
Lethal hit
Adaptive defenses
Cytotoxic
T cell (TC)
Cellular immunity
1 TC binds tightly to
the target cell when it
identifies foreign antigen
on MHC I proteins.
Perforin
TC cell
membrane
Target
cell
Target
cell
membrane
Perforin
pore
Granzymes
3 Perforin molecules
insert into the target
cell membrane,
polymerize, and form
transmembrane pores
(cylindrical holes)
similar to those
produced by
complement
activation.
4 Granzymes enter the
target cell via the pores.
Once inside, these
proteases degrade
cellular contents,
stimulating apoptosis.
Figure 21.20a
by direct contact
by inhibitory cytokines
Cell-mediated
immunity
Humoral
immunity
Inhibits
Inhibits
Triggers
Adaptive defenses
Innate defenses
Surface Internal
barriers defenses
Ag-infected
body cell engulfed
by dendritic cell
Becomes
Ag-presenting cell
(APC) presents
self-Ag complex
Activates
Free Ags
may directly
activate B cell
Antigenactivated
B cells
Clone and
give rise to
Activates
Nave
Nave
CD8
CD4
T cells
T cells
Activated to clone
Activated to clone
and give rise to Induce and give rise to
co-stimulation
Memory
cytotoxic T cells
Activated
cytotoxic
T cells
Memory
helper T cells
Activated
helper
T cells
Memory
B cells
Plasma cells
(effector B cells)
Secrete
Cytokines stimulate
Nonspecific killers
(macrophages and
NK cells of innate
immunity)
Antibodies (Igs)
Circulating lgs along with
complement mount a chemical
attack on the Ag
Figure 21.21
Fig. 43-16
Humoral (antibody-mediated) immune response
Gives rise to
Engulfed by
Antigenpresenting cell
Stimulates
B cell
Helper T cell
Cytotoxic T cell
Memory
Helper T cells
Memory B cells
Memory
Cytotoxic T cells
Active
Cytotoxic T cells
Secreted
antibodies
Defend against extracellular pathogens by binding to antigens,
thereby neutralizing pathogens or making them better targets
for phagocytes and complement proteins.
Interleukin-2 Cytotoxic
stimulates T cell
cell division
Cell-mediated
immunity
(attack on
infected cells)
Interleukin-2
APC
Helper
T cell
activates
other T cells
and B cells
B cell
Interleukin-1
activates
helper T cell
Humoral
immunity
(secretion of
antibodies by
plasma cells)
Figure 24.13B
Organ Transplants
Prevention of Rejection
GVH
Immunodeficiencies
Congenital/acquired
SCID genetic
Acquired Immunodeficiencies
AIDS
Caused by human immunodeficiency virus (HIV)
transmitted via body fluids blood, semen, and
vaginal secretions
Blood transfusions
Contaminated needles
HIV:
AIDS
Attachment
AIDS
AIDS
Treatments include:
Autoimmune Diseases
Multiple sclerosis
Myasthenia gravis
Graves disease
Glomerulonephritis
Rheumatoid arthritis
1.
2.
Gene mutations
Hypersensitivities
Immediate Hypersensitivity
Immediate Hypersensitivity
Immediate Hypersensitivity
RX: epinephrine
Anaphylactic Shock
Constriction of bronchioles
Treatment: epinephrine
Immediate or Type I
Hypersensitivity
Requires sensitization
Sensitization stage
1 Antigen (allergen)
invades body.
IgE mediated
2 Plasma cells
produce large
amounts of class
IgE antibodies
against allergen.
3 IgE antibodies
attach to mast
cells in body tissues
(and to circulating
basophils).
Subsequent (secondary)
responses
4 More of
same antigen
invades body.
Antigen
5 Antigen combines
with IgE attached
to mast cells (and
basophils), which
triggers degranulation
and release of histamine
(and other chemicals).
Histamine
Outpouring of
fluid from
capillaries
Release
of mucus
Constriction of small
respiratory passages
(bronchioles)
Figure 21.21
Subacute Hypersensitivities
Subacute Hypersensitivities
Developmental Aspects
Developmental Aspects