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Host Defense > Lecture 16: Immune Complex Diseases > Flashcards

Lecture 16: Immune Complex Diseases Flashcards

1
Q

What is a hypersensitivity disease?

A

an exaggerated or misdirected immune response

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2
Q

What are the 4 types of hypersensitivity diseases?

A

1 - allergies/asthma
2 - diseases caused by antibodies
3 - diseases caused by antigen/antibody complexes (lupus)
4 - TMMIs

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3
Q

Why is “hypersensitivity reactions” an archaic way to think about these diseases?

A

it implies that a single type of immune cell or molecule is the mediator

(not true - ex: lupus is probably a problem with abnormal TLR activation and faulty Tregs in addition to excess IC formation)

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4
Q

What is type 1 hypersensitivity disease?

A

Allergies/asthma

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5
Q

What is type 2?

A

autoimmune

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6
Q

What is type 3?

A

IC

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7
Q

What 3 things does the formation of ICs depend on?

A

1) source and intensity of antigen exposure
2) rate of IC formation
3) vigor of B cell response

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8
Q

What 2 inflammatory amplifying systems are activated by ICs?

A

1) FcR crosslinking and activation

2) complement via classic or direct pathway

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9
Q

Once activated, what do the antibodies do?

A

generate interleukins, chemokines, prostaglandins to mobilize neutrophiles to site of IC formation

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10
Q

What do Fc receptors recognize, immune complexes or free antibody?

A

ICs! (except armed mast cells with empty IgE)

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11
Q

How do ICs promote beneficial immune responses and inflammation?

A

enhance phagocytosis of encapsulated organisms by binding them to C3b receptors on neuts and macs and crosslinking FcR on same cells and promoting uptake/cell activation

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12
Q

What happens if the rate of neut/mac disposal is exceeded by IC formation?

A

free IC binds to CR1 RBC receptors via C3b and are transported to liver and spleen (then stripped of the complex in the liver or disposed of in spleen)

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13
Q

Where is CR1 (the receptor for C3b) expressed?

A

On all peripheral blood cells except platelets

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14
Q

How many copies of CR1 does the red cell have? white cell?

A

RBC: 400
WBC: 50K

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15
Q

How many more RBCs are in the blood than WBCs?

A

1000x

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16
Q

What happens to C3b when it binds to RBCs?

A

becomes iC3b (inactivated) and is then transported to liver/spleen for disposal

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17
Q

What is the first step of IC formation?

A

form in the circulation and activate complement (complex binds to C1q)

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18
Q

What is the second step in IC processing?

A

coated in bound C3b

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19
Q

What binds to CR1 on the RBCs?

A

C3b

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20
Q

What removes the immune complex in the spleen and liver?

A

phagocytic cells (macrophages, etc)

21
Q

What happens when net IC formation > net destruction?

A

Free ICs will activate multiple inflammatory amplifying systems-especially Fc activation and complement

(will wreak havoc on endothelial layer which is loaded with Fc and C3 receptors)

22
Q

Why is IC disease (Type 3) systemic?

A

because free ICs bind to C3b and Fc

23
Q

What dictates the pathology of immune complexes?

A

site of FcR cross linking

24
Q

What do ICs do when inappropriately bound to vasculature?

A

activate neuts and macs

release IL8 and proinflammatory cytokines that recruit more inflammatory cells to the area

destroys underlying vascular architecture and tissue damage

25
Q

Normal IC processing includes binding to RBCs, true or false? (or is this an arthus?)

A

True, NOT an arthus, this is normal processing

26
Q

What constitutes and Arthus reaction?

A

Too much antibody around so cells are immediately overwhelmed (ex: vaccinating people who already have antibodies to the disease so their immune system is poised and ready to respond)

27
Q

What is special about camel antibodies?

A

have only 2 heavy chains and no light chains

28
Q

What is the pathology of lupus?

A

ICs bind to Fc and C3b receptors on glomerular basement membrane

29
Q

Does detecting and quantifying circulating complexes predict IC disease?

A

NO!!!!

best option is to measure activated C3

30
Q

What are 3 methods of treating IC disease?

A

1) eliminate antigen (antibiotics)
2) inhibit antibody formation
3) suppress inflammation

31
Q

True or false: IC and bound complement fragments delivered to the spleen/lymph nodes or formed in situ in lymphoid tissue are potent stimuli for Ab production

A

True

32
Q

What is the signal that the B cell has achieved its goal?

A

Fc cross linking by antigen-IgG

33
Q

Why would ICs bound to RBCs (via CR1) go to the spleen vs the liver?

A

to immune activation of B cell systems to complexed antigen (liver just removes complexes via Kupffer cells)

34
Q

ICs cause inflammatory reponses by crosslinking FcyR and stimulating the release of ______

A

IL-8 (to recruit neutrophils)

becomes a problem when liver cannot keep up and IL-8 is abundant on site

35
Q

Arthus reactions require what?

A

high levels of pre-existing antibodies

36
Q

What are the symptoms of Arthus reactions?

A

pain, swelling, redness at site of antigen injection

37
Q

What would you think if you detected decreased levels of C3 and C4?

A

direct activation of complement pathway has occurred

38
Q

What is the best treatment for IC diseases?

A

removal of the antigen via antibiotics

39
Q

What is the signal for a mac, monocyte, neutrophil, or DC to phagocytose an IC complex once it binds to the FcR?

A

ITAM (immunoreceptor tyrosine-base activation motif)

40
Q

What happens if the IC binds to a B cell FcR? What is expressed to handle it?

A

ITIM (inhibitory motif) to shut down further B cell proliferation

(this keeps a control on the surplus of antibody already produced)

41
Q

What is characteristic of an infection that leads to activating ITIM?

A

there are a lot of ICs because it binds to the B cell FcR with LOW affinity (unlike the high affinity to the APCs)

42
Q

What is a great example of how the ITAM vs ITIM response can be exploited clinically?

A

the Rh problem!

when Rh is expressed on RBCs and mom is Rh-, she will make antibodies to it for the next pregnancy. If significant antibodies (IgG especially) are made, it will kill the next babies RBCs)

43
Q

What is Rhogam?

A

anti-IgG Rh

it is given to mom during and after her pregnancy (72 hours) to prevent her from making her own IgG Rh antibodies. These synthetic ones will bind to B cells FcR and activate ITIM to cease the production of IgG Rh antibodies

44
Q

How does the Rhogam trick the mom’s immune system?

A

basically tells her she has already made antibodies to Rh so she never generates Rh specific CD4 or B memory cells

45
Q

Is it important that Rhogam is IgG and not IgM?

A

YES! IgM will not work, mom will become sensitized to Rh antigen on fetal blood cells

46
Q

What is another clinical application of exploiting ITIM?

A

give IV IgG to patients suffering from autoimmune diseases - it will turn their own response off hopefully

(or wouldn’t it activate something else?)

47
Q

What is a caveat of administering IV IG during autoimmune responses?

A

it will induce long lasting CD4 and 25 Tregs which will suppress or slow future sensitization

48
Q

True or False: ITIM is only on B cells

A

TRUE

ITAM is only on APCs

Host Defense (21 decks)

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