EXAM II Flashcards

1
Q

List the principal components of innate immunity:

A
  1. Physical & Chemical barriers
  2. Phagocytic Cells, DCs, NK Cells, etc.
  3. Blood proteins (complement system, APP, Cytokines, Chemokines, etc.)
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2
Q

What is the function the complement system?

A

Plasma proteins that complements the ability of Abs & Phagocytic cells to clear pathogens

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3
Q

Define cytokines

Define chemokines

A

Signaling molecules that aid cell-cell communication

Chemokines - subfamily of cytokines that induce chemotaxis

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4
Q

T/F; Innate Immunity is highly diverse

A

False; you are born with what you already have whereas in adaptive, it “adapts” to what the body is exposed to

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5
Q

Which immune response has reactivity to self?

A

Neither

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6
Q

List cells of innate immunity

A
Neutrophil
Monocyte, MO
NK cell
Mast cell
Eosinophil
Basophil
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7
Q

State the main differences between cell-mediated and humoral adaptive immunity

A

Cell-Mediated: intracellular (i.e. viruses), ran by T-helper cells which activate MO & Cytotoxic T-cells

Humoral: extracellular, ran by B-lymphocytes, blood and mucosal secretions, use the help of CD4 T Cells

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8
Q

State the clonal selection hypothesis

A

Ag-specific clones of lymphocytes develop before and are independent of exposure to Ag

Happens twice? During maturation and after Ag exposure

Clone = a lymphocyte of one specificity & its progeny

Clonal Selection allows for a max potential of recognizing diverse microbes

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9
Q

Which disease was involved during the formation of vaccines?

A

Smallpox

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10
Q

List the cells of adaptive immunity

A

B Lymphocytes

T Helper cells

Cytotoxic T cells

T Regulatory cells - suppress and prevent immune responses

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11
Q

List the steps and cell types during B lymphocyte activation

A

Naive B lymphocytes, respond to soluble Ag in secondary organs

Helper T cells present peptide Ags

Stimulated B cells proliferate in germinal centers of LN & mature into plasma cells or memory cells

Plasma cells are terminally differentiated & produce & secrete large amounts of Abs (rarely found in blood)

B cells in spleen respond to polysaccharides

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12
Q

What are the two fates/types of cells in which naive T cells develop into once they are activated by Ag?

A

Memory T cells

Effector T cells

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13
Q

List the steps of T cell activation, what are the two fates of differentiation?

A

Naive T cells enter LN and differentiate into effector or memory T cells which migrate to periphery

Some remain in LN helping Ag-activated B cells

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14
Q

Classical vs. Plasmacytoid DCs

Follicular DCs (unrelated)

Inflammatory DCs

A

Classical - (skin, mucosa, organ parenchyma) once activated migrate to LN

Plasmacytoid - early responders to viral infections, recognize nucleic acids & produce soluble proteins type I interferons (IFN alpha/beta); antiviral activities

Follicular - display unprocessed Ags for B Cell recognition only. DOES NOT INTERNALIZE Ag

Inflammatory - via circulating monocytes

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15
Q

What is the major effect of inflammation?

A

Recruitment of leukocytes and plasma proteins from the blood to the site of infection or tissue injury

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16
Q

What occurs when damaged endothelial cells are activated by cytokines (secreted by resident immune cells)?

A

Adhesion molecules are expressed, causing an increased adhesiveness for myeloid leukocytes and effector and memory lymphocytes

17
Q

Steps of leukocyte recruitment at damaged tissue sites

A
  1. Tethering - selectins & integrins w/ their ligands
  2. Rolling - chemokine interaction
  3. Adhesion - integrins & receptors
  4. Transmigration
18
Q

List the four types of integrins, what cells are they located on?

A
  1. LFA-1; lymphocyte function-associated Ag 1 = Neu, Monocytes, T cells (naive, effector, memory), Naive B cells
  2. Mac-1; MO-1 Ag = MO, DC, Neu.
  3. VLA-4; very late Ag 4 = Monocytes, T cells (all 3)
  4. Alpha4-Beta7; Mono, T cells, B cells (gut homing)
19
Q

What ligands are associated with each of the 4 integrins?

A
  1. LFA-1 = ICAM-1/CD54, ICAM-2/CD102; endothelium; cytokine induced
  2. Mac-4 = ICAM-1, ICAM-2; endothelium; cytokine induced
  3. VLA-4 = VCAM-1/CD106; endothelium; cytokine induced
  4. alpha4-beta7 = VCAM-1, MadCAM-1; endothelium in gut & gut-associated lymphoid tissues
20
Q

Function of integrins?

A

Mediate adhesion of cells to other cells or ECM via specific ligands

Heterodimeric cell surface proteins w/ 2 noncovalently linked polypeptide chains

Activated in response to chemokine binding to chemokine receptors

“Inside-out signaling”

21
Q

What is the basic mechanism in which innate immune cells recognize self vs. nonself?

What cell receptors recognize these?

A

Used by phagocytes and PMNs to initiate phagocytosis

PAMPs - pathogen associated molecular patterns

Recognized by PRRs - Pattern Recognition Receptors

22
Q

What are the 3 receptors of PRR (pathogen recognition receptors)? These are encoded in germline (found in gamete producing cells of the host

A

Toll-like receptor - activate inflammation

N-formylmethionyl receptor (fMet) - found in proks only

Mannose receptor

23
Q

What are the 5 TLRs that recognize extracellular pathogens?

A

TLR-1 = bacterial lipopeptides

TLR-2 = bacterial peptidoglycan = gram (+)

TLR-4 = LPS = gram (-)

TLR-5 = bacterial flagellin

TLR-6 = bacterial lipopeptides

24
Q

What are the 4 TLRs that recognize ingested microbes in the endosomes?

A

TLR-3 = dsRNA

TLR-7 = ssRNA

TLR-8 = ssRNA

TLR-9 = CpG DNA

25
Q

Define necrosis, what 3 DAMPs do they release which activate NF-kB?

A

A passive, catabolic cell death in response to external toxic factors

Damage-associated molecular patterns

  1. HSP
  2. UA
  3. HMGB1

Bind to DCs activating NF-kB pathway for inflammation

26
Q

Define Cathelicidins, what produces them? In response to what?

A

Antimicrobial peptides; activate leukocytes, direct toxicity to microorganisms, bind and neutralize LPS

Produced by neutrophils and barrier epithelial cells in skin, GI, resp. tract

In response to cytokines and microbial products

27
Q

Which component of complement system is the most abundant in the blood?
Strongest chemoattractant?

What is MAC attack?

A

Blood - C3
Chemoattractant - C5a

C5bC6-C9

28
Q

What 2 Abs are involved in the activation of the classical pathway of the complement system?

A

IgM
IgG

Forms an Ab-Ag complex with C1q (binds Fc portion) and C1r, C1s

29
Q

What three things activate each of the complement systems?

A

Classical = Ab

Alternative = microbe

Lectin = mannose binding lectin

30
Q

What are the many functions of pulmonary surfactant proteins SP-A and SP-D?

A
  1. Act as opsonins
  2. Inhibit bacterial growth
  3. Directly activate MO
  • contain lipophilic properties
31
Q

What two components can activate the Lectin pathway of the complement system?

A
  1. MBL - mannose binding lectin

2. Ficolin (humoral plasma proteins) - binds N-acetylglucosamine

32
Q

List the proteins that regulate complement, what are their functions?

A
  1. DAF or CRI - enhance dissociation of C4bC2a (classical & lectin C3 convertase)
  2. CRI and FI - cleave C4b and C3b
33
Q

What are the products of papain and pepsin digestion of Ab?

A

Papain - cleaves above Hinge = 2 Fabs, Fc receptor w/ Fc fragment

Pepsin - cleaves below Hinge = single bivalent Ag-binding fragment (Fc portion is entirely cleaved)

34
Q

Define Ab valency vs. Avidity

A

Valency - (1 Fab region = monovalent, bivalent (IgG), etc.) the max # of Ag determines that can react.

High valency = high affinity

Avidity - Ag-Ab complex strength; high avidity with high amount of binding sites (quantity) = IgM (low affinity)

35
Q

What is the function of HLA-DM during MHC II development?

A

Ensures the presentation of only the most relevant Ags for eliciting an immune response

Causes dissociation of CLIP from peptide binding groove

Stabilizes and prevents degradation of the empty MHC II