Week 9 Part 2

Question 1

HAPTONS-

Answer 1

together with proteins theywork with auto antigens

Question 2

-certain drug reactions

Answer 2

When we take medications, we never know how they react since the immune system of everyone is different.
Production of Abs against the combination of drugs
It occurs very often.
He saw a case with neutropenia (decreased neutrophils in
circulation) because the medication in conjunction with proteins antineutrophils
No neutrophils infection
This is one of the dangers of the medical profession. (Tylenol hasmany bad side effects)
Medications serve like HAPTONS

Question 3

pemphigus vulgaris

Answer 3

Pemphix greek word= blister, bubble
There is a specific type of protein whose function is to work like
a glue between epidermis and deeper layers of the skin=
desmosomal proteins- keep proteins together (located between epidermis and dermis)
In this disease there is production of Abs against these proteins
Leads to disappearance of these proteins and nothing can keep
the skin layers together blisters.
If theres escapes of too much fluid from the blood to the blister

Question 4

desmosomal proteins

Answer 4

Keep proteins together (located between epidermis and dermis

Question 5

Antibody dependent cell mediated cytoxicity

Answer 5

-there is not activation of complement
-no phagocytosis
-it has its own mechanism of formation: in the circulation there are blood cells which have Receptors for FC portion of Ab. When thre is
binding of Ab to AG the FC protion is still open to surrounding
-if the body contains cells with receptors to the FC portion, the
immunoglobulin can bind lysis of target cell without phagocytosis

Question 6

CELLS THAT CAN DO 2

Answer 6

non T/ non B lymphocytes known as natural killer cells (NKC)

• monocytes/ macrophages
• neutrophils
• eosinophils

Question 7

Against…

Answer 7

• only against IgG and iGE

- usually only IgG (the FC receptor will be for IgG only)

Question 8

THIS HAPPENS WITH:

Answer 8

• parasites
• virus infected cells
• tumor cells

Question 9

-myasthenia gravis

Answer 9

-an autoimmune disease that affects the musculature.
-normally: there is spread of the conduction from nerves to the muscle atthe motor end plate. There is ACH that is released from vesicles into the
presynaptic space. The ACH has special receptors on the muscle.when
ACH binds to receptors on muscle contraction

Question 10

antibody mediated
cellular
dysfunction

Answer 10

• myasthenia gravis
• hashiomoto’s thyroiditis
• grave’s disease
• pernicious anemia

Question 11

-hashiomoto’s thyroiditis

Answer 11

-most common cause of hypofunction of thyroid gland in the USA*
HYPOTHYROIDISM
-normally the endocrine works together and they are under the control othe pituitary gland.
-there is negative feedback
-in this disease (the first discovered autoimmune disease in japan)

Question 12

-grave’s disease

Answer 12

-hyperfunction of the thyroid gland
-autoimmune disease, females are more common (20-25 years old)
-production of Abs against the receptors for TSH but in this case the Absstimulate the receptor (they do not simply block it, they permanently
stimulate them) (AB replaces TSH)
-dramatic increase of metabolic rate.

Question 13

-pernicious anemia

Answer 13

• same mechanism of development as graves
• one of the Abs produced are auto Abs knowing as binding ABS who bind to receptors for intrinsic factor
• vit B12 can not go to the blood circulation
• this is an autoimmune disease as well**

Question 14

Systemic

-type 3 (immune complex mediated type)

Answer 14

hypersensitivity reaction is mediated by the deposition of antigen- antibody (immune) complexes, followed by complementactivation and accumulation of polymorphonuclear leukocytes

Question 15

-everything in type 3 (binding of Abs takes place in the blood)

Answer 15

1.-there is an AG in the blood, which leads to formation of AB. They meet in the blood and form an immune complex (IC) in the blood.
2. -after a while they flow with the blood, then they stop to flow because they bind to the
wall of the vessels. (we don’t know why they bind in some tissues and not in others)
3-the function of the immune system is to bind the intruder and eliminate it through
phagocytosis.
-complement potentiates the process of phagocytosis.

Question 16

VASCULITIS-

Answer 16

inflammation of vascular wall

 Vasculitis occurs due to damage of the vessel wall due to enzymes.

Question 17

-serum sickness

Answer 17

Is a reaction to proteins in antiserum derived from a non-human animal source, occurring 4-10 days after exposure.
If someone has bacteria, you put in the serum with Abs and the Abs should bind thebacteria and the person should recover.
But, serum contains a lot of proteins that aren’t self for the recipient body. (these
proteins are seen as intruders) there will be formation of Abs against the proteins
of the serum and this is known as SERUM SICKNESS.
Horses can produce a huge amount of Abs
Uses the HAPTON mechanism. (binds to proteins in the blood and the serum servesas AGs)

Question 18

FAVOURITE SITES OF IMMUNE COMPLEXES DEPOSITION

Answer 18

small vessels
Kidneys 
Joints 
Heart 
Serosal surfaces (peritoneum- abdomen, pleural-chest, pericardium-heart) 
Skin (dermatitis)

Question 19

Glomerulonephritis

Answer 19

Develops independent of serum sickness
 Remember that it may be associated with type 2/3 depending on what causes it***
-usually there is development of IgG/ IgM (classical pathway)
-only these two immunoglobulins are able to bind to complements.
-iGA may have the same result. (alternative pathway)
-decreased serum level of complement in the blood circulation Serum means the plasma without fibrinogen.
 Plasma is the fluid portion of the blood.
 Serum can be taken from the blood and stored.

Question 20

Local

Answer 20

-this is another type of type 3.

Question 21

ARTHUS REACTION

Answer 21

defined as a localized area of tissue destruction resulting from acute immune complex vasculitis.

• inject AG into the skin so you have a high concentration of AG in one small area of the skin.
• but the Abs recognize it as an AG and the Abs try to flow to the area so there is a hugeconcentration of Abs there too and there is formation of AG AB IC.
• there is IC inflammation which leads to tissue necrosis in this area.

Question 22

AN EXAMPLE LIKE ARTHUS REACTION IN HUMANS.

Answer 22

farmer’s lung.

Question 23

farmer’s lung.

Answer 23

-one disease associated with this is found in farmers that work with hay. When the mold on hay is inhaled, the patient makes lots of Abs and after the next encounter with hay
there is another reaction.
-the farmer will die after
-they inhale the dust from the hay and this is dangerous.

Question 24

-type 4 (cell mediated type)

Answer 24

HSR, cell mediated immune response with sensitizedlymphocytes ultimately leads to cellular and tissue injury
type 4 the cells are not Abs (there is no participation of Abs)

Question 25

Type 4 subtypes

Answer 25

delayed type HSR

t cell mediated cytotoxicity

Question 26

delayed type HSR

Answer 26

-when the antigen comes to the human body CD4 and T cells of the TH1 type (other uses TH2) cytokines (IFN-gamma) recruitment of macrophages.
-macrophages are the major effector cells of delayed type HSR.
IFN-gamma~key mediator

Question 27

-autoimmune hemolytic anemia

Answer 27

Characterized by the wrong reaction of the immune system against the RBC when there is production of Abs against theRBCs.
Results in destruction of RBCs
There are many of these anemias