chapter 6 Flashcards

1
Q

What are features of innate immune

A

nonspecific

no memory

does not change with antigenic exposure

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2
Q

What does the innate immune system manifest as

A

inflammation

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3
Q

What are the 6 PRR?

A
  1. TLL
  2. Nod-like receptors
  3. GCPRs
  4. C-type lectin receptors
  5. Mannose-binding lectin receptors
  6. ROD-like receptors
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4
Q

Where are the following receptors located?

  1. TLL
  2. NOD-like receptor
  3. C-type lectin receptors (CLR)
  4. GCPRs
  5. ROD-like receptors
A
  1. plasma membrane and endosome
  2. Cytosol of necrotic cells
  3. Plasma membrane of MO and DCs**
  4. neutrophils, MO and most leukocytes
  5. Cytosol
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5
Q

What are the 3 responses of the innate immune system?

A
  1. inflammation
  2. protect against viruses using Type-1 interferons
    • the adaptive immune respronse
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6
Q

Adaptive immunity develops later and is stronger. It is mediated by lymphocytes, which have specific receptors for antigens, and antibodies. Consists of 2 types:

what types of microbes do they respond to?

A
  1. Humoral immunity; mediated by B cells and anitbodies and respond to EXTRACELLULAR microbes
  2. Cell-mediated immunty is mediated by T-cells and responds to INTRACELLULAR microbes
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7
Q

What is clonal selection?

A

B4 lymphocytes respond to an antigen, they are already specific for certain antigens.

Lymphocytes will then bind to that antigen and activate/ make more that are specific that that antigen.

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8
Q

What are our generative (primary/central) lymphoid organs?

A
  1. BM

2. Thymus

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9
Q

What occurs in BM and thymus

A

BM: hematopoiesis (BM, leukocytes and plasma cells are made) and B-cells mature (become naive)

Thymus: T -cel mature (become naive)

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10
Q

What is located in peripheral organs (secondary) and what occurs?

A

lymphocytes, APC and antigens

immune response

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11
Q

What are 3 examples of peripheral organs

A

LN

spleen

MALT

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12
Q

What occurs in LN

A

lymphocytes interact with antigens in circulation and undergo clonal expansion

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13
Q

what occurs in spleen

A

lymphocytes interact with blood borne antigens

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14
Q

MALT is made up of tonsils, adenoids and peyers patches) and is located where?

What is the purpose of it?

A

under the epithelial of skin, resp, GI tract

Allows lymphocytes to be near antigens of the mouth and GI tract

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15
Q

How are B cells organized in LN?

What happens when B cells are activated

A

In follicles located peripherally with follicular DC, which present the antigen to them

A germinal center is created in the middle

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16
Q

How are T cells located in the LN

A

Paracortex around follicles.

DC in the paracortex present antigen

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17
Q

Lymphocyte recirculation is important for what cells?

A

T cells.

Mature the thymus into naive T-cell => peripheral lymphoid organ, where they will meet up with antigen => become effector T-cell which then goes to the site of infection

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18
Q

why is lymphocyte less important to B-cells

A

Plasma cells stay in the lymphoid organ.

Follicular DCs present antigen to them and then they make AB that are secreted to go tothe site of infection

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19
Q

Where are antigens concentrated

A

lymphoid organs

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20
Q

in the case of immunization with a protein antigen, microbial mimics, called _____, are given with the antigen and these stimulate the ____ immune response

A

adjuvents

innate

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21
Q

When does a lymphocyte stop being naive?

A

when an antigen binds

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22
Q

When antigen binds, what happens

A

becomes:

  1. effector cell
  2. memory cell
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23
Q

Lymphocytes can respond to multiple antigens, but what is the catch?

A

They can only be of 1 type!

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24
Q

CD4+ Helper T cells

recognize what?

that are presented on what MHC, causing what to happen?

What is the action of what aoocured

A

Extracellular antigens (bacterial and allergens)

MHC Class II, located ONLY on APC=> release of cytokines

  1. Activate MO => phagocytose
    • T and B cells
  2. Recruit leukocytes => inflammation
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25
Q

CD8+ CTLs

recognize what?

that are presented on what MHC, causing what to happen?

What is the action of what aoocured

A

Intracellular antigens (viral and tumors)

MHC Class I, located on all nucleated cells => secrete cytokines

Cytokines released will kill intracellular antigen

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26
Q

T-REG CELLS AXN

A

SUPRESS IMMUNE RESPONSE AND PREVENT SELF ANTIGEN

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27
Q

where are mature T-cells located?

A
  1. blood (bc recirculate; 60-70% of lymphocytes)

2. T cell zone of peripheral lymphoid organs

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28
Q

Describe the TCR

A
  1. TCR heterodimer: binds the antigen; 95% is ab
  2. CD3 and zeta chains: noncovalently linked and are signal transducer; identical in all T-cells
  3. CD4 ORRRR CD8+
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29
Q

How much of circulating lymphocytes are mature B=cells ?

A

10-20%

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30
Q

Where are mature B-cells located?

A

LN, spleen and MALT

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31
Q

What receptors and ligands are involved in CD4+ helper T-cells activating B-cells?

A

CD40 on B cell

CD40L on helper T-cell

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32
Q

How can the compliment system that occured in innate immunity activate B-cells?

A

Compliment products made during innate immunity will bind to CR2/CD21 receptors on the B cells.

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33
Q

What part of the BCR is relavant in hyper IgM syndrome?

A

CD40

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34
Q

DCs are the MOST IMPORTANT cells for initiating a ___-cell response.

What features of it allow it to do so?

A

T-cell

  1. Expresses many receptors to recognize antigens
  2. Expresses high levels of MHC
  3. Go to peripheral LN in response to microbes
  4. Located in epithelium and intersitium, where many antiges are made
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35
Q

Follicular DCs are found in _________ of lymphoid follicles in what peripheral lymphoid organs, where they do what

A

germinal center

spleen and LN

present to B-cells

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36
Q

Follicular DCs ahve receptors for which receptors that bind antigens

A

IgG

C3b

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37
Q

What are the 3 important actions of MO?

How are they important in cell-mediated immunity?

What about humoral-mediated immunity?

A
  1. Phagocytosize and present to T-cell
  2. kill ingested microbes
  3. important in humoral immunity bc that phagocytosize and destroy microbes that were opsinized by IgG and C3b.
38
Q

What is GM makes Classic cards mean?

A

IgG and IgM coat pathogens => activate the classical compliment pathway

39
Q

Function of CD16 found of NK cells?

A

ADCC (antibody-dependent cell-mediated cytotoxicity)

NK cells have CD16, a Fc receptor for IgG.

  1. NK cell uses CD16 to recognize cells coated in IgG => kills them
40
Q

How do we control whether a NK cell will kill

A

Has activating and inhibiting receptor

+ receptor: NKG2D will recognize a damaged cell with virus/tumors that do NOT have class I receptor

  • receptor: + of NK cell is inhibited if a cell has Class I MHC, which is present on all nucleated cells
41
Q

actions of NK cells (3)

A
  1. Recognize damaged cells (virus or tumor) and release perforin to kill => MO will then eat it up
  2. Release IFN-y => + M1 macrophages to destroy intracellular microbe
  3. ADCC: uses CD16 receptor to rexognize and kill antigens coated with IgG
42
Q

What activates NK cells?

What do NK cells rlease nad what does it do?

A

IL2 and IL15

IL12 => + TH1 cells => IFN-y => + M1 MO

43
Q

What does IL12 do?

A

+ TH1 cells => IFN-y => activate M1 MO to destroy intracellular microbe

44
Q

Innate lymphoid cells?

what was the first defined ILC

actions

A

lack TCRs, but secrete cytokines

look like lymphocytes, but act like cells in innate imunity

NK cells

  1. early defense in infection
  2. Stress survailence
  3. release cytokines to help with T -cell differnetiation
45
Q

MHC are encoded on Chromosome 6 and they’re HIGHLY polymorphic

do they function primarily in adaptive or innate immunity?

A

adaptive

46
Q

MHC class 1 is made up of what?

Where are they located?

______ is encoded by what 3 genes?

A

heterodimer: a heavy chain and B2 microglobulin

on all nucleated cells and platelets

alpha heavy chain is encoded by HLA A/B/C

47
Q

MHC Class 1 displays what antigens?

Binding groove?

Binding co-receptor

TM domain

A

Intracellular viral/tumors that were derived from proteins and presented as peptides

binding groove: a1 and a2

binding co-receptor: a3 (nonpolymorphic) has a binding spot for CD8+

tm domain: B2-microglobulin

48
Q

MHC class 2 is made up of what?

Where are they located?

encoded by?

A

a-chain and b-chain

located on all APC: B cells, DCs and MO

HLDA-D has 3 subregions: DR/DQ/DP

49
Q

MHC Class 2 displays what antigens?

Binding groove?

Binding co-receptor

TM domain

A

extracellular antigens (bacterial and allergy) and soluble proteins that were internalized into vesicles

binding site: a1 and B1

binding co=receptor: B2 has a binding site for spot for CD4+

50
Q

How are MHC class I and 2 complexes different in how they preesnt their antigens?

A

MHC Class I (intracellular)

  1. Intracelullar proteins => proteosomes, where they are broken down into peptides
  2. => ER, where they load onto a1/a2 binding groove of HLA-A/B/C
  3. HLA combines with B2 globilin to form a stable trimer => moves to surface

MHC Class II (extracellular bacteria and allergies and ingested proteins)

  1. taken up into vesicles
  2. go to endosome, where they are broken down into peptides by endosomal enzymes
  3. combine with HLA-DQ/R/P and form a vesicle
  4. go to surface
51
Q

Main function of innate immune system is: inflammation and - viral replication

Cytokines are released mainly by what cells?

What are these cytokines?

A

MO, DC and neutrophils

IL1, 12, type IFN, IFN-y and TNF

52
Q

Main function of adaptive immune system is: increase lymphocytes, differentiation and activation

Cytokines are released mainly by what cells?

What are these cytokines

A

CD4+ T cells

IL2, 4, 5, 17, IFN-y

53
Q

Main function of hematopoeisis is to increase leukocytes and replace them

What releases what cytokines to stimulate hemotopoeiss?

A

Marrow, stroma, T cells and MO

GM-CSF and IL-7

54
Q

which Igs have the shortest and longest half life

A

shortest: IgE
longest: IgG

55
Q

Which IgG goes across placenta

A

IgG

56
Q

IgE does what

A

binds to mast cells, eso, basophils with high affinity => kill parasites

57
Q

when are mast cell sensitized in type 1 reactions

A

when IgE binds to the surface

58
Q

Besides the second exposure of the allergen to mast cell in Type 1, what else can + the mast cell

A

C3a
C5a
==> mimic anaplaxais

59
Q

Immediate phase of type I occurs minutes after d/t the release of what

A
  1. vasoactive amines (histamine, enzymes and proteoglycans)

2. lipid mediators (leukotriene B4-E4, prostaglandin D2, PAF)

60
Q

What does Leukotriene B4 do

A

recruit eosinphils, neutrophils and monocytes

61
Q

What are the most potent VASOACTIVE and BRONCHIOSPASMIC AGENTS?

A

Leukotriene C4, D4, E4,

62
Q

What is the most abundant mediator made by mast cells? what does it do?

A

prostaglandin D2

causes bronchospasm and increase mucus secretions

63
Q

What lipid mediator is released in immediate type I reactions, but is the only one not made from AA?

A

Platelet activating factor

64
Q

Sx in early phase response of type 1 reaxtion

A

vasodilation

edema

smooth muscle contraction

mucus secretion

65
Q

why do local immediate phase reactions occur at the sites that they do?

A

Mast cells are located IN tissue NEAR BV, nears and subepithelial tissues.

66
Q

How are basophils and mast cells different?

A

similar (both have IgE receptors and granules in cytplasm,

, but they are NOT in tissue, they circulate in blood.

67
Q

What found inside Mast cells helps us to visualize them histologically?

A

Acidic proteoglycans which bind basic dyes such as touidine blue

68
Q

Late phase occurs 2-24 hours later and is d/t the release of what?

A

cytokines and leukotrienes

69
Q

What is the late phase characterized by

A

infiltration of the tissue with

eosinphils*****
neutrophils**
basophils*
monocytes 
CD4+ T cells 

and epithelial tissue damage

70
Q

What do eosphilis do?

A

release
major basic protein,
proteolytic enzymes,
cationic protein

THAT DAMAGE MUCOSAL EPITHELIAL TISSUE

71
Q

Which cytokines released by Mast cells and their functions?

A
  1. TNF, IL-1 and chemokines => recruit leukocytes (which is key in late phase response)
  2. IL4 => increases TH2
72
Q

Sx in late phase:

A

mucosal epithelial cell damage allergic rhinits and asthma

73
Q

[Q:] Which mediators are responsible for the intense immediate reactions characterized by edema, mucus secretion, and smooth muscle spasm?

A

histamine

leukotrienes

74
Q

[Q:] Which mediators set the stage for the late-phase response by recruiting additional leukocytes?

A

cytokines and chemokines

75
Q

Patient comes in with a type I hypersensitivity rxn. how do we treat?

A

early phase: anti-histamines (EPI)

late phase: anti-inflammtory drugs

76
Q

[Q:] What molecule is chemotactic for eosinophils?

A

• eotaxin

77
Q

Genetics and environment are big players in our predispostion to allergies. describe them

A

Genetics
1. Atopy: increased propensity to devvelop immediate hypersensitivity reactions: high IgE and IL-4

  1. Mut on Chr 5, which encode cytokines in reaction
  2. Mut on Chr 6, located near HLA complex

Evn: may be more imp?
Non-atopic allergy: allergy caused by non-antigenix stimuli that do NOT involve IgE or TH2: it is through that we get these bc our mast cells are ABNORMALLY SENSITIVE to non-immune stimuli

78
Q

Systemic anaphlaxis key sz

A
  1. Vascular shock
  2. widespread edema
  3. diff breathing

A. itching, hives, uticaria

B. bronchoconstriction and laryngeal edema (hoarse)

C. V/D, cramps and laryngeal obstruction

D hypotensive shock and death can occur in min- hours

79
Q

Type 3 reactions (other name)

Reactions tend to be what? Although, what?

D/t:

A

SYSTEMIC -immune complex mediated

systemic, although, immune complexes seen to accumulate in the [kidney, lungs, skin and joints].

  1. too many exogenous antigens present (acute serum sickness)
  2. endogenous antigens (lupus)
  3. infectios diseases
80
Q

Type III Hypersensitivity preferentially involve what 3 organs/sites?

causing what?

A
  1. Kidneys => glomerulonepritits
  2. small BV => vasculitis
  3. Joints => arthritis
81
Q

What AB are usually involved in type 3

A

IgG

IgM

82
Q

In step 3 of Type 3 sensitivity;

Inflammation and tissue injury
1. About 10 days after antigen introduction –> classical compliment system is activated => producing anaphylatoxins (C3a, 4a and 5a), attracting leukocytes (neutrophils) to immune complex, which release enzymes and causes what?

A

acute inflammatory rxc =>

  1. fever
  2. joint pain (arthralgia)
  3. proteinuria
  4. lymphadenopthy
  5. uticaria
83
Q

What is the difference between serum sickness and arthus reaction?

A

Serum sickness => systemic reaction

Arthus reaction=> local reaction

84
Q

When single large non-protein antigen is introduced to the body, it caues a acute, self-limited diseases that goes away as the antigen is elimianted. When the antigen is removed, it is it goes away. What is this caused and what are examples

A

acute serum sickness

diptheria anti-toxin and post-strep glomerulonephritis

85
Q

When single large non-protein antigen is introduced to the body, but the exposure is prolonged and causes chronic recurrent tissue injury. What is this called and what are examples

A

chronic serum sickness

lupus; a persistant AB response to autoantigens

86
Q

inflammatory reaction caused when you inject antigen at a specific site in a previously immunized animal that has AB for the antigen

=> forms local immune complezes => localized necrosis and vasculitis

A

arthus reaction (experiment)

87
Q

What is the morphology of type 3 mediated diseases

A

fibrinoid necrosis and nucleophilic infiltration

88
Q

immunofluorescene of type 2 reactions will look how?

A

smooth and linear d/t deposits of immunoglobulin and compliment

89
Q

immunofluorescene of type 2 reactions will look how?

A

grainy and lumpy

90
Q

How will post-streptococcal differ in the <3 and kidney?

How will this differ on immunoflurosences

A

Post-step in the HEART => is a type 2 reaction => look smooth and linear

Post-strep in the KIDNEY => type 3 reaction and will look grainy