First Aid Immunology Flashcards

1
Q

IgG

A
main antibody in secondary (delayed) response to antigen. Most abundant isotype in the serum. 
Fixes complement 
Crosses the placenta (passive immunity)
Opsonizes bacteria 
Neutralizes bacterial toxins and viruses
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2
Q

IgA

A

Prevents attachment of bacteria and viruses to mucous membranes. DOES NOT fix complement. Monomer in circulation, but dimer with J chain when secreted. Crosses epithelial cells by transcytosis. Produced in GI tract Peyers patches and protects against gut infections like giardia.

It is the most produced antibody overall, but low serum levels.

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3
Q

IgM

A

Produced in the primary (immediate) response to an antigen. Fixes complement, does not cross the placenta. It is the antigen receptor on the surface of Bcells. Monomer on the B-cell, but a pentamer with J chain when secreted.

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4
Q

IgD

A

unclear function

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5
Q

IgE

A

Binds mast cells and basophils. CROSS LINKS when exposed to antigen. Mediates type hypersensitivity through the release of inflammatory mediators such as histamine.

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6
Q

Acute Phase Reactants

A

factors whose serum concentrations change in response to inflammation. Produced by the liver in both acute and chronic inflammatory states. Notably: induced by IL-6.

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7
Q

Important cytokines secreted by MACROPHAGES

A

IL-1 - causes fever, acute inflammation, activates endothelium to express adhesion molecules.

IL-6 - Causes fever and stimulates production of acute phase proteins.

IL-8 major chemotactic factor for neutrophils “clean up on aisle 8”

IL-12 - induces differentiation of T-cells to Th1.

TNF- alpha - mediates septic shock. activates endothelium. Causes WBC cell recruitment. Vascular leak.

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8
Q

Important cytokines from Th1 cells

A

Interferon-y - stimulates macrophages to to kill phagocytosed pathogens. Inhibits differentiation of Th2. Increases MHC expression and antigen presenting cells.

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9
Q

Important cytokines from Th2 cells

A

IL-4 - induces differentiation of T cells into Th2. Promotes B-cell growth. Enhances class switching IgE to IgG.

IL- 5 - promotes growth and differentiation of B-cells. Enhances class switching to IgA. Stimulates growth and differentiation of eosinophils.

IL-10 - ATTENUATES inflammatory response. Decreases expression of MHC class 2 and Th1 cytokines. Inhibits 
--> NOTE both TGf-beta and IL-10 attenuate the immune response.
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10
Q

Superantigens

A

(i.e. strep pyogenes, s aureus) cross link the B-region of the tcell receptor to the MHC complex on APCs. this can activate CD4 tcell leading to a massive release of cytokines.

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11
Q

endotoxins

A

i.e. lipopolysaccharide gram negative bacteria. DIRECTLY stimulate macrophages by binding to endotoxin receptor TLR4/CD14, Th cells are not involved.

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12
Q

Classic examples of antigenic variation

A
Salmonella - 2 flagellar variants 
N gonorrhea pilus protein 
Viruses: 
HIV 
Flu
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13
Q

Live attenuated vaccine

A

microorganism with retained pathogenicity, but capacity for transient growth in innoculated individual. CELLULAR and HUMORAL response.

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14
Q

Inactivated or killed vaccine

A

pathogen inactivated by heat or chemicals. maintaining surface epitope. mainly induces humoral response.

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15
Q

Important live attenuated vaccines

A

intranasal flu
mmr
varicella
yellow fever

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16
Q

important killed vaccines

A

flu IM
rabies
polio
hep A

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17
Q

anti ACh receptor

A

myasthenia gravis

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18
Q

anti basement membrane

A

goodpastures

19
Q

anticardiolipin, lupus anticoagulant

A

SLE, antiphospholipid antibody syndrome

20
Q

anticentromere

A

limited scleroderma (CREST syndrome)

21
Q

CREST syndrome

A
Calcinosis 
Raynauds 
esophageal dysmotility 
scleroderma 
telangectasia
22
Q

anti-dsDNA, anti-smith

A

specific for SLE

23
Q

anti-glutamic acid decarboxylase (GAD65)

A

Type 1 diabetes

24
Q

antihemidesmosome

A

bullous pemphigoid

25
Q

anti-histone

A

drug induced lupus

26
Q

anti-jo, anti-SRP, anti-MI-2

A

polymyositis, dermatitis

27
Q

anti-thyroglobulin

A

hashimotos thyroiditis

28
Q

anitmitochondrial

A

PBC

29
Q

antinuclear

A

SLE sensitive

30
Q

anti-parietal cell

A

pernicious anemia

antibodies to intrinsic factor?

31
Q

anti-scl-70 (topoisomerase)

A

systemic scleroderma

32
Q

anti-smooth muscle

A

autoimmune hepatitis type 1

33
Q

Anti-SSA(Ro), Anti-SSB(La)

A

Sjogrens

34
Q

Anti-TSH

A

graves disease

35
Q

voltage gated calcium channel antibodies

A

Lambert Eaton

36
Q

IgA anti-endomysial IgA anti-tissue transglutaminase

A

Celiac

37
Q

c-ANCA

A

GPA (Wegener)

38
Q

p-ANCA

A

MPA

eGPA (Churg strauss)

39
Q

Rheumatoid factor (IgM to IgG Fc region), anti-CCP

A

rheumatoid arthritis

CCP more specific

40
Q

Transplant rejection: Hyperacute

A

Within minutes. pre existing recepient antibodies react to donor antigen. Type II hypersensitivity. Activate complement.
–> Widespread thrombosis of vessels.
remove the graft.

41
Q

Transplant rejection: Acute

A

weeks-months.
Cellular: Type IV hypersensitivity reaction, CD8 tcells activated against donor MHCs.

There is also Humoral acute rejection. antibodies develop AFTER transplant.

Can prevent/reverse this process with immunosuppression.

42
Q

Transplant rejection: Chronic

A

CD4 tcells respond to recipient APCs presenting donor peptides, this includes allogenic MHC. Both cellular and humoral (Type II and IV component).

43
Q

Transplant rejection: Graft vs host disease

A

Grafted Tcells proliferate in the immunocompromised host and reject host cells a “foreign protein”. Type IV hypersensitivity.

Symptoms: maculopapular rash, jaundice, diarrhea.

Usually in bone marrow and liver transplants as these are rich in lymphocytes.