Download 43.3 Active and Passive immunity Active Immunity Passive Immunity

43.3 Active and Passive immunity
Active Immunity
- Immunity obtained from recovering
from an infectious disease Ex.
Chickenpox. Depends on the
response of individual’s OWN immune
system. Naturally acquired
- If immunity is via immunization
then called artificially acquired. Ex.
Vaccinations. Body retains Ags to
stimulate immune response and
memory. Antigenic variability of
pathogen is a big factor in
determining success of vaccine. That
is why some require boosters and
others are a onetime deal.
Passive Immunity
- Antibodies transferred from one
individual to another. Ex. IgG from
mother to fetus across placenta and
IgA in colostrum.
- Only lasts as long as Abs last (few
weeks to few months).
Artificial –is when the Abs are injected from an immune animal/person to a
nonimmune animal/person. Ex. Gammaglobulins.
Natural – is when Abs transferred from mother to fetus across placenta.
Concept 43.4
ABO and Rh blood groups. Table 43.1.
Blood group
Ag on RBCs surface
A
A
B
B
AB
Both A and B
O
Abs made
B
A
Neither
That’s why AB is
universal acceptor
Both A and B
Neither A or B
That’s why O is
universal donor
Q: How does an A person make Abs to B and a B person make Abs to A?
A: Abs arise in response to normal flora bacteria having epitopes very similar
to blood group Ags. Blood group Ags are polysaccharides, which induce T –
independent responses therefore no memory cells made. So, each response
like the primary response. Generates IgM anti-blood group Abs. NOT IgG so
good as IgM cannot pass across placenta so if fetus is a different blood
group to mother it is not harmed.
Q: Rh factor?
A:
Is a protein antigen on RBCs, so if a small amount of fetal blood crosses the
placenta IgG made.
Rh factor causes trouble as Abs are IgG and so pass across placenta. If
mother is Rh negative (no Rh factor) and fetus is Rh positive (from Dad), and
fetal blood leaks across placenta, as it may during later stages of pregnancy
or delivery, then T-dependent humoral response against Rh factor
generating antibodies to Rh and memory B cells.. Danger is for later
pregnancies as mother’s Rh specific B memory cells are exposed to the Rh
factor resulting in IgG Abs that cross the placenta and destroy red blood
cells of fetus. To stop this the mother is given anti-Rh Abs after delivery
of first Rh positive baby and so she has received passive immunization to
destroy Rh+ red blood cells, so no memory cells created.
MHC molecules are responsible for graft vs. host reaction in tissue and
organ transplants. The MHC molecules of donor and recipient need to be
well matched to avoid rejection. Only same in identical twins. Recipients are
given immunosupression drugs to suppress Th cell activity and leave nonspecific and T-independent humoral responses alone so that patient has
some immune responses.
Concept 43.5 Exaggerated / Diminished IRs:
Allergies:
• Hypersentivity to environmental Ags = Allergens.
• Possible explanation is leftover evolutionary immune response to
parasites such as worms.
• Most common ones involve IgE (Fig. 43.18).
• Plasma cells secrete IgE for allergen
• IgE attaches by tail to mast cells in connective tissue without binding
pollen
• Later pollen enters and binds antigenic site on IgE molecules on mast
cells
• Trigger degranulation of mast cells Fig. 43.20.
• Histamine and other inflammatory agents released
• Acute allergic reaction results in anaphylactic shock (widespread mast
cell degranulation (Phoebe and the Florida wasp!).
Autoimmune Diseases:
• When Immune system turns on “self.” Autoantibodies made to
histones and DNA that are released normally when cells
breakdown.
• Depending on which molecules involved determines the disease:
a) Lupus – Abs against histones and lots of self-molecules. Results in
skin rashes, fever, and kidney dysfunction).
b) Rheumatoid arthritis – damage and inflammation of cartilage and
bone of joints.
c) Insulin-dependent diabetes mellitus – beta cells of pancreas are
destroyed. These produce insulin to convert glucose to glycogen.
d) MS – T cells attack myelin sheath of neurons.
• Causes are varied and complex. A lot is unknown.
• Inheritance of particular MHC molecules?
• Failure in immune system regulation.
B. Immunodeficiency disorders:
• If caused by a genetic or developmental defect = inborn/primary
immunodeficiency (ID). Ex. SCID ( Severe Combined Immuno
Deficiency).
• SCID has both branches of IS fail to work. No humoral or cellmediated arm. Need a BM transplant. One type of SCID has
defective adenosine deaminase leads to build up of toxic substances
for B and T cells. Gene therapy has been used to introduce functional
adenosine deaminase gene and has been successful in a child.
• If develops later following exposure to a chemical or agent = acquired
or secondary ID. Ex. Hodgkin’s, AIDS.
• Hodgkin’s disease, which damages the lymphatic system. IS
suppressed by cancer so lymphatic system damaged.
• In either one person gets recurrent infections and more susceptible
to cancer.
• As many disorders as there are components of the immune system.
• Certain cancers suppress the immune system.
• Can vary from temporary states due to stress to devastating condition
such as AIDS.
C. Healthy immune system depends on the endocrine and nervous systems
functioning properly. Endocrine secretes hormones and nervous system uses
neurotransmitters. Both are affected by stress, emotions and health of the
individual. Hormones from adrenal glands affect the number of WBCs. Some
neurotransmitters are released when person is relaxed, happy – may enhance
immune system.
D. AIDS:
• Immunodeficiency disease caused by a virus.
• Strains HIV 1 and HIV 2.
• HIV 1 is the most widely found and most virulent.
• Infect T cells with CD4 ( Th), use CD4 as receptor to gain access to
cell. Also, coreceptor ( fusin on all HIV infected cells). Different
ones on Th and Macrophages. Both are chemokine receptors.
• CD4 also on macrophages and some B cells.
• Co receptors on Th and macrophages used for chemokine attachment
therefore people with defective chemokine receptors immune to HIV.
• HIV mutates frequently therefore a challenge to the cell-mediated
and humoral arm of immune system.
• IS still able to make Abs resulting in an early immune response.
• Detection of these Abs is basis of HIV test but show up weeks to
months after infection!
• HIV replication occurs in cells of lymph nodes resulting in damage to
these cells and the HIV levels in the blood go up but Th numbers go
down!
• Causes of T cell depletion unknown – HIV interactions induce apoptosis
of Th cells?
• Opportunistic diseases are ones that take advantage of a
compromised immune system Ex:cancers, bacterial and viral infections
that a normal healthy person would easily fight off.