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Transcript
The Immune System
Immunity
 = the body’s ability to resist infection
 can be natural or acquired
Pathogens
disease causing microorganisms





bacteria
virus
fungi,
protozoa,
parasite,
 allergens
Three Lines of Defense
How does the body fight infection/foreign
invaders?
The Body has 3 lines of Defense
First Line of Defense – The Skin
•
Provides Physical and Chemical barriers
 Physical – hard to penetrate, made of indigestible
keratin
 Chemical – tears, sweat
First lines of defense
saliva
antibacterial
enzymes
(lysozymes)
skin
prevents
entry,
bacteria
stomach acid
low pH kills
harmful
microbes
tears
antibacterial
enzymes
(lysozymes)
mucus linings,
cilia traps dirt
and microbes
Bacterial
flora - out
compete bad
Second Line of Defense – Nonspecific Immune
Response
Includes:
 Phagocytosis – done by Macrophages (neutrophils and
monocytes)
 Natural Killer Cells (NK) – secretes perforins (cytolitic)
 Inflammation - caused by release of Histamine from
leukocytes
 Fever – caused by histamines and pyrogens. The fever (high
temp) kills invaders and decreases their growth by denaturing
their proteins.
Phagocytes
Phagocytes
 Monocytes and macrophages
 Provide a non-specific response to
infection
 http://www.microbelibrary.org/imag
es/tterry/anim/phago053.html
Phagocytosis
Pus
An accumulation of :  dead phagocytes
 destroyed bacteria
 dead cells
Third Line of Defense
 Specific response –
(Immunity)
 lymphocytes produce
antibodies that target specific
pathogens
Lymphocyte
Lymphocytes
Provide a specific immune response to
infectious diseases.
2 types:
- T-cells –mature in thymus
- B-cells mature in bone
marrow then are found in
lymph nodes and spleen
They circulate in blood and lymph and produce
antibodies.
Antigens
 all cells have surface
markers called
antigens.
 Large and complex
proteins,
polysaccharides,
glycoproteins, or
glycolipids
 body can recognize
these as self or nonself (foreign)
Specific response
 Lymphocytes detect presence of foreign
antigens
 Stimulated to produce
specific proteins called
antibodies.
How an antibody works?
Deactivation of a bacterium by an antibody = primary response.
Macrophages – Antigen presenting
cells (APCs)
Antigen becomes
part of the MHC
(major
histocompatibility
complex)/HLA
(human leukocyte
antigens)
*Used for
transplant
compatibility.
The Pathway of Specific Immune Response
Step 1
Pathogens eaten by
Macrophage
Step 2
Displays portion of
Pathogen on surface
Step 3
Pathogens
Helper-T cell
recognizes
Pathogen
T-Lymphocytes
 have receptors with similar structure to
antibodies and are specific to 1
antigen.
 activated when the receptor comes
into contact with the antigen with
another host cell (e.g. on an APC)
T-Lymphocytes
 After activation the cell divides to form:
 Helper T cells – secrete CYTOKINES
 help B cells divide and produce antibodies
 stimulates macrophages
 Activates cytotoxic T cells
 Cytotoxic T cells (killer T cells)
 Kill body cells displaying antigen
 Bind to APC and release perforins
 Memory T cells
 clones that remain in body for future immunity
B –Lymphocytes
(humoral/fluid response,
antibody-mediated)
 10 million different B-lymphocytes, each
make a different antibody
 Receptors in the membrane recognize
the antigen on the surface of the
pathogen or APC, cytokines released by
helper T cells
the activated B-cell
divides rapidly.
B -Lymphocytes
 Some activated B cells  PLASMA
CELLS and produce lots of antibodies,
~ 1000/sec
 The antibodies travel to the blood,
lymph, lining of gut and lungs.
 The number of plasma cells goes
down after a few weeks
 Antibodies stay in the blood longer
but eventually their numbers go down
too.
B -Lymphocytes
 Some activated B cells  MEMORY
CELLS.
 Memory cells divide rapidly as soon
as the antigen is reintroduced.
 There are many more memory cells
than there were clone cells.
 When the pathogen/infection infects
again it is destroyed before any
symptoms show.
Activates Cytotoxic
Cytokines!
Activates B- Cell
T- Cell
perforins
Memory T-Cell
Kills Infected
Memory B-Cell
Antibodies
Cellular Immunity .vs. Antibody Immunity
Cellular Immunity
 Carried out by TCells
 Infected cells are
killed by Cytotoxic T
–Cells.
Antibody or Humoral
Immunity
 Carried out by Bcells
 Antibodies are
produced and
dumped into blood
stream.
 Antibodies bind to
antigens and
deactivate them.
Immune Response Explained
1.
2.
3.
4.
5.
6.
7.
8.
9.
Antigen infects cells.
Macrophage ingests antigen and displays portion on its
surface.
Helper T- Cell recognizes antigen on the surface of the
macrophage and becomes active.
Active Helper T-Cell activates Cytotoxic T-Cells and BCells.
Cytotoxic T-Cells divide into Active Cytotoxic T-cells and
Memory T – Cells.
Active Cytotoxic T-Cells kill infected cells.
At the same time, B-Cells divide into Plasma Cells and
Memory B- Cells.
Plasma cells produce antibodies that deactivate
pathogen.
Memory T and Memory B cells remain in the body to
speed up the response if the same antigen reappears.
Immune Response Summary
Displays copy of
antigen on surface of
cell
Antigen
Macrophage
Cellular Immunity
Helper T - Cell
Active Cytotoxic T-Cell
Kills Infected Cells
Memory T- Cell
Antibody Immunity
Active B - Cell
Plasma Cell
Antibodies
Deactivates Antigens
Memory B-Cell
Primary .vs. Secondary Immune Response
 Primary Immune Response
 This is a response to an invader the First
time the invader infects the body.
 No measurable immune response for first few
days.
 Next 10 – 15 days antibody production grows
steadily
 Secondary Immune Response
 A more rapid response to an invader the 2nd
time it invades the body.
 Antibody production increases dramatically and in
a much shorter time period..
Antibodies
 Also known as immunoglobulins
 Globular glycoproteins
 The heavy and light chains are
polypeptides held together by disulphide
bridges
 The order of amino acids in the variable
region determines the shape of the
binding site - variable
How Abs work
 Some act as labels to identify
antigens for phagocytes
 Some attach to bacterial flagella making
them less active and easier for
phagocytes to engulf
 Some cause agglutination (clumping
together) of bacteria making them less
likely to spread
 Increase inflammation to prevent spread
Different Immunoglobulins
Type
Number of
ag binding
sites
Site of action
Functions
IgG
2
•Blood
•Tissue fluid
•can cross placenta
•Increase
macrophage activity
•Antitoxins
•Agglutination (antiRh)
IgM
10
•Blood
•Tissue fluid
Agglutination
Ex-food antigens
IgA
2 or 4
•Secretions (saliva,
tears, small intestine,
vaginal, prostate,
nasal, breast milk)
•Stop bacteria
adhering to host
cells
•Prevents bacteria
forming colonies on
mucous membranes
IgE
2
Tissues
•Activate mast cells
 HISTAMINE
•Worm and allergy
Immunological memory
 after an infection is fought off some
lymphocytes become memory cells.
 if same pathogen returns memory cells stimulate
the produce the specific antibody very rapidly.
 the infection is fought off before symptoms
appear = secondary response
 vaccines can stimulate same response
Primary .vs. Secondary Immune Response
Passive .vs. Active Immunity
1. Active Immunity
This is immunity where the body is “actively” producing
antibodies to fight infection.
Ex: You have a throat infection and you are actively
creating antibodies to fight it.
Vaccination:
An injection of a weakened strain
of an infectious microbe (pathogen) that causes the
body to undergo active immunity (produce
antibodies).
2.
Passive Immunity
This is immunity where antibodies are given to
a person from the blood of another person or
animal.
This immunity only lasts for a short period of
time.
ex: Breastfeeding mothers pass antibodies to
their children through the milk.
Vaccination
A preparation containing antigenic
material:
 Whole live microorganism
 Dead microorganism
 Attenuated (harmless) microorganism
 Toxoid (harmless form of toxin)
 Preparation of harmless antigens
Allergies
 When the immune system responds to harmless
substances
 Allergens – antigenic substances which do no real
harm
 Allergens include house dust, animal skin, pollen,
house dust mite and its faeces
 There are two types of allergic reactions.
a. Immediate – occurs within seconds and normally
lasts for about 30 mins.
b. Delayed – takes longer to react and can last for a
much longer time.
What happens during an allergic reaction?

During an allergic reaction antibodies cause histamines to
be released from certain cells.
Histamines cause:
a. Swelling of tissues
b. Release of fluids (runny noses and eyes)
c. Muscle spasms (some cases)
Example: TB (Mantoux test)
Allergies
 Histamine causes blood vessels to widen
and become leaky.
 Fluid and white blood cells leave capillaries.
 The area of leakage becomes hot, red and
inflamed
Anaphylaxis or anaphylactic shock:
This is the sudden and severe allergic reaction to
a substance that can cause death.
-inherited tendency to over-produce IgE (evolved to
protect against round and flat worm infection)
Treatments for Allergies
1. Avoidance of material – especially food.
2. Epinephrine – “epi – pen”
3. Antihistamines -- benadryl
Autoimmune Disease
 Autoimmune diseases are diseases where the
immune system begins to attack itself.
 Ex:
 Rheumatoid Arthritis – crippling disease of
the joints.
 Lupus – disease of blood and organs.
 Multiple Sclerosis – disease of nervous
system
 Cause(s): mostly unknown; virus alters
proteins,T cells don’t differentiate properly; a
nonself may resemble a self antigen
 More common in females –fetal cells transport
through circulation and cause later response
 Cures/Treatments: No known cures. Usually
treated with drugs.