Intro To Immunity And Inflammation Part II Flashcards

1
Q

What are the functions of antibodies

A
  • neutralize and aggluntinate antigens
  • tag/identify specific invaders for phagocytosis (opsonization)
  • activate complement
  • enhance NK-cell activity
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2
Q

What kind of protection is IgG?

A

Long term

Secondary immune response

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3
Q

What is the only antibody that crosses the placenta?

A

IgG

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4
Q

What do all of the antibodies do

A

Neutralize and agglutinate

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5
Q

IgD

A

Defective, intermediate

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6
Q

How many epitope can IgM bind?

A

10

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7
Q

IgE

A

Allergies and worms

-gets bored and binds to things causing allergies if not exposed to other things for it to “do”

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8
Q

What antibody crosses the mucous membrane

A

IgA

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9
Q

Which antibody is present the most in secretions?

A

IgA mostly

Some IgM and IgE

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10
Q

What is the predominant antibody in the blood?

A

IgG

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11
Q

What antibody can cross placenta

A

IgG

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12
Q

Which antibodies activate complement

A

IgG and IgM

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13
Q

What antibody reacts with neutrophils and macrophages mostly?

A

IgG (some IgA)

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14
Q

What antibody reacts with basophils and mast cells?

A

IgE

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15
Q

Why don’t you want IgA in GI?

A

Activates complement which activates inflammation, don’t want inflammation in the GI

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16
Q

Secondary immune response and past infection Is class?

A

IgG

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17
Q

Primary immune response and acute infection Ig class?

A

IgM

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18
Q

Largest antibody

A

IgM

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19
Q

Antibody class associated with allergies

A

IgE

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20
Q

Immunological response in nutshell

A
  • microorganissms penetrate innate barriers
  • macrophage ingest and present antigen
  • Ag activates specific memory Th and B cells
  • antibodies and plasma cells that produce them are specific to a single antigen
  • after battle, only a few memory B cells and T cells are left on guard for that antigen
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21
Q

What does HIV attach

A

CD-4 directly

Takes out immune systems traffic cop

22
Q

Primary immune response-1st exposure

A
  • requires 1-2 weeks post first exposure
  • antibody response not long lived
  • symptoms of illness occur during this time (acute phase)
  • antigen selected B and T cells need time to proliferate and differentiate into effector cells
23
Q

Time you have a pathogen and no antibodies to attack it in primary immune response

A

Viral window

24
Q

What 3 things describe the primary immune response

A
  • delayed
  • robust
  • IgM
25
When do B cells make antibodies in the primary immune response?
Whenever they become plasma cells, they cannot produce antibodies until then
26
Secondary immune response -subsequent exposures
- hours to days to occur - greater magnitude response and more prolonged - occurs due to presence of memory cells - IgG
27
How do you differentiate actute illness from a past illness with antibodies
Measure IgM
28
Is allergic response primary or secondary?
Secondary, you have to have been exposed before to have an allergy to it
29
What antibody class is secondary response predominated by
IgG
30
Blood is drawn from a patient presenting with symptoms of hepatitis. The test ordered include hepatitis A antigen, anti hepatitis A (IgM), anti hepatitis A (IgG), hepatitis B antigen, anti hepatitis B (IgM) and anti hepatitis B (IgG). Lab results are ``` Hep A Ag- neg anti-hep A (IgG)-neg Anti-hep A (IgM)-neg Hep B Ag-POS Anti Hep B (IgG)-neg Anti-hep B (IgM)-POS ``` What is your interpretation?
Acute and recent because antigen still present and presence of IgM
31
Subject actively produces their own antibodies. Requires exposure to infections agent again
Active
32
Natural active
Natural infection
33
Artificial active
Immunization with altered agent or its antigens | -immunizing with killed agent. Cannot determine if active or passive until know what you were immunized with
34
Subject receives exogenous antibodies. Does not confer long term immunity
Passive
35
Passive natural immunity
Mother child (IgG-placenta)
36
Artificial passive immmunity
Immunization with antibodies - when we want them to have immediate protection - such as a snake bite and rabies - don't have time to wait for own antibodies to be produced - this is both active and passive!
37
Hazards of immunity
- inadvertent injury to the host - development of autoimmunity - hypersensitivity reactions
38
Body sites and tissues that are immune privileged
- Eye - Brain: ventricles and striatum - pregnant uterus - testes and ovary - adrenal cortex - hair follicles - hamster cheek pouch - certain tumors
39
Hypersensitivity reactions
ACID - type I: allergy/immediate - type II: cell-bound/cytotoxic - type III:immune complex - type IV: delayed
40
What kind of responses are all of the ACID hypersensitivity reactions
Secondary responses and more than one can take place at the same time
41
Which hypersensitivity reactions ate antibody mediated
Type I, II, III
42
What type of hypersensitive reaction is cell mediated
Type IV: delayed
43
What is the only hypersensitivity reaction that is mediated by IgE?
Allergy/immediate (type I)
44
Mechanism of type I (allergy/immediate) reaction
Allergen cross links mast cell-bound IgE, triggers degranulation
45
Clinical presentation of type I hypersensitivity reaction
Anaphylaxis, atopy, asthma, hives, hay fever
46
Clinical presentation of type II hypersensitivity reaction (cell-bound/cytotoxic)
Transfusion reaction, immune hemolytic anemia, erythroblastosis fetalis, graves, myesthenia gravis, graft rejection
47
Mechanism of type II (cell-bound/cytotoxic) hypersensitivity reaction
Complement-activating contibodies (IgM/IgG) bind to cells and trigger lysis
48
Clinical presentation of type III hypersenitivity reaction (immune complex)
Serum sickness, arthus reaction, SLE, RA, poststeptococcal glomerulonephritis, farmers lung, vasculitis
49
Mechanism of type III hypersensitivity reaction (immune complexly)
Circulating immune complexes contains complement fixing antibodies (IgG)
50
Which types of hypersensitivity reactions use complement
Type II and III
51
Clinical presentation of type IV (delayed) hypersensitivity reaction
TB skin test, contact dermatitis, celiac disease, type I DM, MS, graft rejection
52
Mechanism for type IV (delayed) hypersensitivity reaction
Sensitized lymphocytes