Transcript Dynamic Defense System

Dynamic Defense System
Ch 43 Notes
Pathogens
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Infectious Agents that cause disease
Viruses, bacteria, protists and fungi may be
pathogens
Animals fight back using immune cells
Innate Immunity
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Found in all animals
Active immediately upon infection
Includes: barriers (skin), internal defenses
Made of preset group of receptors that binds
to a molecule absent from animal bodies but
found in microbes
Acquired Immunity
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Found only in vertebrates
Activated after innate immune defense
Enhanced by previous exposure to pathogen
Very specific
Innate Immunity of Invertebrates
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Exoskeleton – first line of defense
– Chitin effective against most pathogens
Lysozyme – enzyme that digests microbial cell walls –
blocks pathogens in digestive system
Phagocytosis – Ingestion and digestion of
bacteria/foreign substances – fights pathogens that get
through exoskeleton
Antimicrobial peptides – circulate through insect bodies to
kill fungi and bacteria
I. Innate Immunity of Vertebrates
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Barrier Defenses
1. Intact skin – barrier that can’t normally be
penetrated by microbes
2. Mucous membranes – line digestive, respiratory
and urogenital tract
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a. Mucus – fluid secreted by mucous membranes – traps
microbes and is removed from body by cilia (tiny hairs)
b. Acid – produced in stomach destroys microbes before
they go into the digestive tract
Lysozyme – destroys bacteria in respiratory tract and eyes
Sweat and oil glands have low pH to kill bacteria
Cellular Innate Defenses
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1. Phagocytic white blood cells
– Use TLR receptors to recognize pathogens
– TLR triggers internal defenses
– Phagocyte traps microbe, engulfs it, makes a
vacuole, fuses with lysozyme, kills microbe
Neutrophils
– Most numerous WBC
– Infected tissue sends signals which call out
neutrophils
– Neutrophils engulf and destroy
Cellular Innate Defenses
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Monocytes
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enter into damaged tissue and form macrophages
attach to microbe’s surface, “eat” it and destroy it
using lysosomes – YUM!!
macrophages live permanently in lungs, liver,
kidney, brain, lymph nodes and spleen
If microbe is in blood – trapped in spleen
If microbe is in interstitial fluid – trapped in lymph
Cellular Innate Defenses
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c. Eosinophils
*defend against large parasites (eeww)
Antimicrobial Peptides and Proteins
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Interferons – proteins that provide defense
against viral infections
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Cells infected with virus sends out interferons
Cause uninfected cells nearby to produces
substances to fight off virus
Limits cell to cell spread
Antimicrobial Peptides and Proteins
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Complement System- 30 proteins in blood
plasma
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Fight infections
Circulate in an inactive state
Get activated by microbes
Causes cascade of reactions leading to lysis of
invading cells
Inflammatory Responses
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Response to tissue damage (from injury) or
to entry of microorganisms
Histamine – released by mast cells at site of
tissue damage
Arterioles dilate (open) and venules constrict
(shrink) so that the blood supply increases in
the area (swelling and redness)
*aid in blood clotting and repair
*block spread of microbes
Inflammatory responses
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During inflammation – signals sent out
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Antimicrobial proteins go to site
More histamine is released
Phagocytes attracted
Neutrophils and macrophages are called in
Ends with accumulation of Pus – filled with
WBC’s, dead microbes and cell debris – YUM!!
Natural Killer Cells
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Help recognize and eliminate certain
diseased cells in vertebrates
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Cells have class I MHC molecules on their
surface
When a virus infects or cell becomes cancerous,
cells stop expressing the MHC protein
Natural Killer cells attach to these damaged cells
and cause them to die preventing spread
Evasion by Pathogens
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Some pathogens can avoid being destroyed
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Some bacteria have capsules that hide
polysaccharides in the cell walls and don’t get
recognized (like strep pneumoniae)
Some bacteria are resistant to breakdown after
phagocytosis (like TB)
Acquired Immunity
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Pathogen specific response
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Specific response to an invader (not general
defense like innate defenses
Acquired Immunity
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Lymphocytes – WBC’s
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2 Types – B lymphocytes (B cells) and T
lymphocytes (T cells)
circulate through blood and lymph and are
concentrated in lymph nodes and spleen
Contribute to Immunological Memory– recognize
and respond to a specific foreign invader that has
been encountered previously
Acquired Immunity
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Antigen – foreign molecule that causes a
response by lymphocyte
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can be found on viruses, bacteria, fungi, protozoa,
parasitic worms
also found on pollen (allergies) and transplanted
tissue (like heart transplant)
B cells and T cells recognize antigens using
Antigen Receptors
Acquired Immunity
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B Cells (form and mature in Bone marrow)
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Produce antibodies that are specific to a particular antigen
*5 classes of antibodies (IgA, IgD, IgE, IgG, IgM)
*Structure of antibodies is basically the same except
for a variable region that makes the antibody
recognize specific antigens
*Antibody binds to intact antigen and inactivates it
*Macrophage comes and eats it
II. Specific Line of Defense –
IMMUNE SYSTEM
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T Cells (form in bone marrow and mature in Thymus
gland)
Only bind to antigen fragments that are on the
surface of host cells
recognize nonself cells
if nonself cell is identified, T cells divide rapidly and
produce
Cytotoxic T cells (killer T cells) that puncture non-self
cells and make them burst
Helper T cells – stimulate more B cells and killer T
cells to form to help fight the invader faster
Acquired Immunity
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T Cell receptors
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Have alpha and beta chain
Also have constant region and variable region
Acquired Immunity
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MHC – Major Histocompatability Complex
Helps immune system tell the difference between
self (you) and nonself (invader)
MHC is unique to all individuals (except identical
twins or clones )
Class I
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found on almost all cells of body
Bind peptide fragments of foreign antigens
If body cell is infected or cancerous, it makes foreign antigens
and displays them
Cytotoxic T cells recognize these antigens and kill the infected
cells
Acquired Immunity
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MHC II
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Made by dendritic cells, macrophages and B cells
Bind to foreign materials that have been taken in
by phagocytosis
Cytotoxic and Helper T cells recognize them
Amplifying Lymphocytes
Binding of an antigen receptor to its specific antigen
initiates events that activate the lymphocyte
B Cells and T cells amplify the response
Effector cells – short lived – attack the antigen and the
pathogens that are making it
Memory Cells – long lived – bear receptors specific for
the antigen
Clonal Selection – proliferation (making lots) of clone
cells in response to an antigen
-Presenting of an antigen to a receptor leads to lots
of cell division = thousands of cells to fight pathogen
Clonal Selection
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Primary Immune Response- takes 10-17
days (when you get sick)
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invader attacks a body cell
antigens from invader bind to a B cell with the
correct receptor
B cell proliferates (makes lots of copies of itself)
and makes two types of cells (effector and
memory)
Clonal Selection
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Secondary Immune Response – takes 2-7
days (usually don’t get sick)
Individual is attacked by same invader at a
later time
T and B memory cells recognize the antigen
much faster and produce a stronger
response (2-7 days)
E. Categories of Immune Responses
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Humoral Response
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involves most body cells
responds to antigens or pathogens circulating in
the blood or lymph fluid
B cells produce plasma cells
Plasma cells release antibodies that bind to
invading antigen
B cells produce memory cells for future immunity
Used for Extracellular pathogens
Cell Mediated Response
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Cell-mediated response
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uses mostly T cells and responds to any nonself
cell triggering the following events:
Cell Mediated Response
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Antigen presenting cell stimulates Cytotoxic
T cell
Cytotoxic T cell becomes activated
Secretes proteins to cause cell rupture and
cell death
Used for Intracellular pathogens and cancer
Also makes memory T cells for future
infection
Role of Antibodies
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Bind to antigen
Interfere with pathogen in different ways
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Bind to pathogen and block it’s ability to enter host
Bind to toxins released by pathogen and neutralize them
Made it easier for macrophage to recognize invader
Use a membrane attack complex to make a hole in the
membrane of the foreign object – cause it to swell and burst