Transcript Immune System - College of Charleston

The Immune System
1. The Innate System
2. The Adaptive System
The Innate Immune System
“Nonspecific” system
– Surface Barriers
– Cell and Chemical Responses
Innate Immunity: Surface Barriers
Innate Immunity:
Cell and Chemical Defenses
• They do not target specific pathogens
– They target abnormal or foreign cells
• Six categories:
–
–
–
–
–
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Phagocytes
Natural killer (NK) cells
Inflammation response
The complement system
Interferons
Fever
Phagocytes
• Macrophages, neutrophils, eosinophils
1. Adherence and endocytosis
2. Phagocytic endosome
3. Lysosome fuses with endosome,
releases hydrolytic acids/enzymes
4. Microbe is killed and digested
5. Exocytosis
Natural Killer Cells
• Lymphocytes that destroy tumor cells and
cells infected with viruses
• Not phagocytes, instead release chemicals
onto cell membranes
– Cytolytic, perforin complexes
• The target cell lyses & nucleus disintegrates
• NK cells also release substances to stimulate
inflammation
Inflammation
Response
•Redness
•Increased
Temperature
•Swelling
•Pain
The Complement System
• > 20 plasma proteins
• Activation triggers cascade
of chemical reactions
• Molecular Complexes
form:
– Membrane Attack Complex
creates holes in bacterial
cell membranes
– C3b marks them for
phagocytes
– C3a and C5a stimulate mast
cells to release histamines
Interferons
- Interfere with viral
replication
- Block protein synthesis
at ribosomes
- Activate macrophages
- Mobilize NK cells
Fever
• When macrophages attack foreign matter,
they release chemicals called pyrogens into
the blood
– Endogenous: interleukins, tumor necrosis factors, macrophage
inflammatory protein, interferons
– Exogenous: Lipopolysaccharides of gram-negative bacteria trigger
endogenous factors
• The hypothalamus is stimulated to increase
body temperature – fever
• Liver and spleen sequester iron and zinc
• High temp. unfavorable for microbes
The Adaptive Immune System
“Specific” defense mechanisms
• Three characteristics:
– recognizes & targets specific foreign
substances
– protects the entire body, not a specific
injury or infection site
– has a "memory" to store information
from past exposures
Cell Recognition
Proteins, polysaccharides, glycoproteins
signal the identity of the cell (host or
foreign)
• Major histocompatibility
complexes (MHC)
– Molecular markers on host cells
• Antigens
– Substances that mobilize the immune
response
• Molecular markers on foreign cells,
abnormal/infected or cancerous host cells
Auto-immune diseases arise when our immune system
cannot differentiate “host” from “foreign” cells
Key to Adaptive Immune System
• Lymphocytes
• Originate from stem cells in bone marrow
• 30% of circulating WBCs
– B cells
• mature in Bone marrow
– T cells
• mature in Thymus Gland
– Both types are made in the bone marrow
– Immune response may be antibody-mediated
(humoral) or cell-mediated
Antibody-mediated Immunity
• Antibodies: Y-shaped
proteins (4 polypeptides)
– Made by mature Blymphocytes
• Binds to antigens to form
antigen-antibody complex
Antibody-mediated Immunity
• Immunoglobulin classes
– IgD: antigen receptor of B cell
– IgM: antigen receptor of B cell
(monomer); released by plasma cells
during primary response (pentamer)
– IgG: most abundant and diverse; targets
bacteria, viruses, toxins; main antibody
for both primary and secondary response
– IgA: found in exocrine secretions;
prevents pathogens from attaching to
epithelial surface
– IgE: bound to mast cells and basophils;
mediates inflammation and allergic
reaction
Antibody-mediated Immunity
Antigen
Pathogen
Antibody-mediated
Immunity
MHC
Macrophage
MHC+Antigen
• WBC detects a pathogen or
abnormal cell
Signaling
molecules
– Attacks pathogen
– Alerts Helper T cells and B
cells
• T cells attracted by chemical
signals
• B cells alerted by using the
pathogen’s own antigens
B cell
Helper T cell
Antibody-mediated
Immunity
• Antigens bind to specific
antibodies on B cell surface
• Activation causes B cells to
divide rapidly
– Plasma cells
• produce antibodies
• 100 million antibodies/hour
– Memory B cells
• Remain on “stand by” until
activated by helper T cells
• Surveillance
Cell-mediated
Immunity
• MHC + antigen
complex waves a
warning flag
• Class II MHC’s found
on B cells, some T
cells, and antigenpresenting cells
• Class I MHC’s found
on most cells, except
RBCs
Antigen
Pathogen
Cell-mediated
Immunity
MHC
Macrophage
MHC +
Antigen
Signaling
molecules
• Helper T cells (CD4):
– recognize class II MHC
– stimulate other immune cells
Helper T cell
• Cytotoxic T cells (CD8):
– recognize class I MHC
– kill infected, cancer, or foreign cells
• Memory T cells:
– reactivate on re-exposure
• Suppressor T cells:
– suppresses other immune cells
Signaling
molecules
Cytotoxic T cell
Activated
Cytotoxic T cell
Perforin
molecules
form pores
in pathogen
cell membrane
Memory
T cell
Cell-mediated Immunity
• Helper T-cells facilitate both cellmediated and antibody-mediated
immune responses
• Cytotoxic T cells function similar to
NK cells, however they only see
specific MHC I + antigen complexes
Memory B and T Cells are Like…
Immune Memory
• Primary immune response
– first exposure to pathogen
– recognition, production of B & T cells
• 3 to 6 day lag time
• antibodies peak in 10 to 12 days
– B & T memory cells created
– basis for "immunity" from the disease
• Secondary immune response
– Memory B & T cells immediately identify the
pathogen
– faster, longer lasting, more effective than the
first
– at subsequent infection, new legions of B & T
cells form in a few days
– often no symptoms are noticed