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Immunology > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

Tolerance: Gut

A

M cells process antigen
taken up by gut dendritic cells
travel to mesenteric lymph nodes- make IL-10, favors Treg development

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2
Q

What is autoimmunity?

A

immune response to self antigen and a loss of tolerance

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3
Q

Is autoimmunity an autoimmune disease?

A

No! But it is a cause of inflammation and when the damage from inflammation exceeds the body’s ability to repair you get DISEASE!

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4
Q

General characteristics of autoimmune disease

A

idiopathic-except when drug induced, suspected that infection/virally induced
multiple factors involved-genes, sex, age, infection
most HLA associated diseases are autoimmune
multiple immune mechanisms
inability to avoid immunogen

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5
Q

Mechanisms of autoimmune disease

A

failure to delete autoreactive clone in thymus
breakdown of peripheral tolerance (loss of anergy)
antigen-nonspecific lymphocyte activation (superantigens)
molecular mimicry-infectious immunogens cross react w/ self
abnormalities in lymphocyte interactions

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6
Q

ideal immune response

A

directed only against harmful immunogens
completely effective and totally eradicates harmful immunogen
completely protective, with no host tissue damage

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7
Q

Latrogenic

A

adverse response to therapy

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8
Q

Mechanisms of tolerance

A

not inherited but acquired=active process
developed during fetal life
requires continued presence of immunogen
induced in adult animals under some conditions
Est. of tolerance as clinical goal: allergy therapy, est of allografts

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9
Q

Central tolerance

A

immunogen-induced apoptosis of double positive T cells (negative selection in thymus)
immunogen-induced apoptosis of IgM-expressing B cells

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10
Q

Peripheral tolerance

A

immunogen-induced anergy in absence of costimulation (during antigen presentation there is no B7-CD28 costimulation)

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11
Q

Induction of tolerance in mature immunogenic reactive cells

A

Treg are distinct helpers, can be antigen specific, produce primarily immunosupressive cytokines-inhibit autoimmune cell function
M2 macrophages and NKreg cells involved
TGFbeta and IL10

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12
Q

induction of tolerance in mature cells, clinically

A

oral tolerance to proteins
high dose tolerance to aq. proteins (system. adm)
low dose tolerance- repeated, low doses (systemic)

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13
Q

alloantigen

A

foreign antigen from same species

ex: ABO blood groups, Rh factors, HLA complex, minor blood group system

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14
Q

Alloimmunity in pregnancy

A

results when mother and fetus have different Rh factors.
1st pregnancy=sensitizing event
2nd+ pregnancies=secondary immune response, lots of high affinity IgG transctosed to fetal circulation causing massive destruction of fetal erythrocytes triggered by anti-Rh IgG
Results in anemic newborn

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15
Q

What medication is used to treat mom with anti-Rh IgG?

A

RhoGAM

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16
Q

What are the hazards associated with blood and blood derivatives?

A

transfusion reactions- hemolytic and febrile

Infection disease- CMV, Hep C, HIV, Hep B

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17
Q

Which blood type is the universal donor?

A

O-

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18
Q

Which blood type is the universal acceptor?

A

AB+

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19
Q

What is the most important thing to match correctly for a blood transfusion?

A

ABO group then RH, minor blood groups and HLA

20
Q

When transplanting an organ or tissue what is most important to match?

A

HLA complex (class 1 > 2)&raquo_space; ABO

21
Q

Why treat a transplant patient with CSA and glucocorticoids?

A

to induce tolerance by suppressing the normal immune response

22
Q

How does cyclosporine work?

A

Cyclosporin works by inhibiting the production of IL-2 which is made by Th1 cells and induces T cell proliferation and promotes cell growth. IL-2 also enhances cytotoxic activities of NK cells and CTL which is seen in graft rejection. Inhibition of IL-2 will lead to a decrease in T-cell proliferation and cytotoxic activities

23
Q

Hyper acute organ rejection

A

preexisting antibody- antibodies against donor blood group antigens bind vascular endothelium of graft, initiating inflammatory response that occludes blood vessels and rapidly causing it to fail.

24
Q

Acute Organ rejection

A

T-cell mediated due to HLA differences
When donor organ is transplanted into recipient some donor dendritic cells are present. After the transplant they migrate to the spleen, activate effector T cells which recognize the Class I and II MHC as foreign and then they migrate to the transplanted organ, inflammation sets in and eventually destroys it.

25
Q

Alternate mechanism for acute organ rejection

A

Direct: CD4 and CD8 effector T cells recognize the nonself MHC on donor DC and attacks
Indirect: antigen is presented to donor DC, processed and present on the surface by foreign MHC and then CD4 recognizes that it isn’t right and attacks!

26
Q

Chronic organ rejection

A

antibody mediated causing decreased perfusion

Increase in inflammatory cells enables immune effectors to enter the tissue

27
Q

How can pregnancy lead to anti-HLA phenotype?

A

mother and father have different HLA

during birth mother and fetal cells mix and stimulates the production of antibodies against paternal HLA

28
Q

transplant rejection

A

when T cells attack the transplant

29
Q

graft vs host disease

A

when the T cells in the donor tissue/organ attack the recipient’s tissue

30
Q

Coombs and Gel Hypersensitivity reaction: Type 1

A

IgE mediated (anaphylactic or immediate)
soluble antigen cross links IgE on mast cells to cause degranulation
(Atopy and rhinitis)

31
Q

Early phase products of Mast cell degranulation

A

Histamine, heparin and TNFa

32
Q

Late phase procucts of mast cell degranulation

A

leukotrienes, PAF, IL-4, IL-13

33
Q

What kind of response is a mast cell degranulation associated with?

A

Th2 response geared to fighting off parasites

34
Q

What receptor binds IgE to Mast cells

A

FceRI

35
Q

What other cells can bind IgE?

A

eosinophils and basophils

36
Q

Coombs and Gel Hypersensitivity reaction: Type II

A

Cytotoxic Allergy

complement activation and ADCC IgG and IgM

37
Q

How does penicillin cause a Type II rxn?

A

it modifies proteins on RBC creating foreign epitopes

38
Q

What are the basics of complement activation?

A

Ab binds to the cell
Ab binds to the Ag
Complement binds to Ab
Complent kills cell

39
Q

How does antibody dependent cellular cytotoxicity work?

A

(NK cells and Macs)
anti-CD20 Ab binds to CD20 on surface of B-cell lymphoma cell
Fc receptors on NK recognize bound anti-CD20 ab
cross-linked Fc receptors signal NK cell to kill the B-cell lymphoma cell
B-cell lymphoma dies by apoptosis

40
Q

Coombs and Gel Hypersensitivity reaction: Type III

A

Immune Complex Disease (IgG)

Highly immune person exposed to high dose of classical complete immunogen

41
Q

Tissues effected by Type III hypersensitivity and type of lesion

A

those w/ small vessels-kidneys, joints, lungs, skin

vasculitis

42
Q

Coombs and Gel Hypersensitivity reaction: Type IV

A

Cell-mediated allergy (delayed hypersensitivity or tuberculin type)
CD4+ T cells- Th17 (promote inflammation response by macs)
CD8+ T cells (tissue rejection)

43
Q

Tissues effected by type IV hypersensitivity

A

skin very common but can be any

allergen ex: nickel, poison ivy, latex

44
Q

Which types of hypersensitivity involve inflammation?

A

Types I, III and IV

45
Q

What is atopy?

A

Inherited tendency for IgE mediated allergy to common environmental allergens, commonly inhalants and ingestants

Immunology (2 decks)

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