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Transcript
Defense against Disease
Non-specific and specific strategies
Inherent Challenges
• Constant surveillance and vigilance
• Unpredictable invaders
The Enemy
• Pathogens: microorganisms that are capable
of causing disease
• Viruses
• Bacteria
• Fungi
Public Enemy #1
The Viruses
•Modus Operandi
Dock with receptors on target cell surface
Insert viral DNA or RNA into host cell
Use host cell machinery to replicate new
viruses
Lyse host cell and spread to nearby cells
•Lytic vs. Lysogenic life cycles
•Examples: smallpox, chickenpox,
polio, HIV
Public Enemy #2
Bacteria
•Modus operandi
Set up shop in tissues but remain
EXTERNAL to cells
Reproduce rapidly
Secrete exotoxins or contain endotoxins
as part of cell wall
•Examples: Escherichia coli,
Clostridium botulinum, Salmonella
Figure from Holt Biosources
Public Enemy #3
Fungi
•Modus Operandi
Similar to bacteriareproduce rapidly
Damage cells directly or indirectly
by secreting enzymes
•Examples: Athlete’s Foot,
Pneumocystis carinii (fungal pneumonia)
http://www.ces.ncsu.edu/depts/pp/bluemold/
So what’s a body to do?
• First line defenses: Nonspecific anatomical
barriers and secretions that prevent entry,
such as skin, saliva, tears (lysozyme),
mucus, stomach acid, fever
• Second line defenses: Inflammation
A nonspecific response triggered by histamine
secreted by basophils when tissue is
damaged
If all else fails…
The Immune Response
• A highly specific, long lasting response tailored to
combat pathogens
• Vocabulary:
Antigen- a molecule (usually carried on the
surface of a pathogen) that is capable of eliciting
an immune response
B-Lymphocytes- white blood cells that produce
and secrete antibodies
T-Lymphocytes- white blood cells that serve as
part of the cell-mediated immune response
Self- Nonself Recognition
• Critical to appropriate immune system function
• Tcells “learn” to distinguish self from non self as
they mature in the thymus
• All nucleated self cells display unique Human
Leukocyte Antigens (HLA) on their Major
Histocompatibility Complex (MHC) receptors
• As T cells mature, they randomly produce and
display a variety of receptors
• Any T cell with receptors that bind to self MHCHLA complexes will commit apoptosis
• Only T cells that do NOT bind to self cells should
emerge from the thymus and enter circulation
The Immune Response - Overview
Immune Response- Step by Step
1. Pathogen (carrying foreign antigens) enters and
survives the inflammatory response
2. Some pathogens remain exposed in tissues
where their antigens may be recognized by
circulating B cells
OR
3. Macrophages engulf pathogens and display their
antigens on MHC (major histocompatibility
complex) receptors. Macrophage has now become
an Antigen Presenting Cell (APC)
Central Role of Helper T Cells
Humoral Immunity
B cell response
• If a circulating B cell’s receptors bind to
foreign antigens, the B cell becomes activated
• Activated B cells divide into Memory B cells
and Plasma B cells
• Plasma B cells rapidly produce and secrete
antibodies (immunoglobulins)
• Clonal selection amplifies the production of
cells that produce effective antibodies
Clonal Selection
Figure from AccessExcellence.org
Mechanism of Antibody Function
• Antibodies bind to antigens
and aggregate pathogens for
removal by macrophages
• Antibodies disrupt function
of pathogen’s surface
proteins
• Antibody-antigen
complexes trigger the
Complement system, a a
series of enzymes carried in
the bloodstream that lyse
invaders
Figure from AccessExcellence.org
Cell-Mediated Immunity
T cell Response
• Helper T cells (a.k.a. TH or CD-4 T cells) constantly
interact with macrophages
• When TH cell finds a macrophage that is presenting
antigen (APC) it becomes activated
• Activated TH cells secrete cytokines, chemicals that
stimulate both T and B cells
• Stimulated cytotoxic T cells (a.k.a. killer or CD-8 T
cells) divide rapidly, bind directly to pathogen
infected cells and secrete enzymes that lyse infected
cells
Cytotoxic T-Cells