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Immunology (By: Ben + Dustin) > Lecture 1&2 Material (Dustin) - Basics & Innate Immunity > Flashcards

Lecture 1&2 Material (Dustin) - Basics & Innate Immunity Flashcards

1
Q

What is clonal selection theory?

A

animal first randomly generates a vast diversity of lymphocytes, and then those lymphocytes that can react against the foreign antigen encountered are specifically selected for action

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2
Q

What is “memory” in terms of immune response?

A

Refers to faster response time with secondary response vs primary response, with same antigen.

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3
Q

What is the main antibody of the primary vs secondary immune response?

A

Primary: IgM dominant

Secondary: IgG dominant

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4
Q

What is an epitope?

A

A portion of the antigen that is recognized by a given T or B cell receptor. Not totally the same definition as an antigen! May be multiple epitopes in one antigen.

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5
Q

How long are MHC-I bound peptides? And MHC-II bound peptides?

A

MHC-I: 8-9 AA’s long
MHC-II: 11-20 AA’s long (slightly longer)

Unfortunately this is important to know

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6
Q

What type of epitopes do antibodies usually recognize?

A

3D structures, aka “conformational epitopes” of native molecules

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7
Q

What is the major difference in the types of antigens that T and B cells initially recognize?

A

B cells can recognize antigens in their native form (the B cell receptor is an antibody), while T cells need antigens to be processed by antigen-presenting cells (they must be linear peptides! more limited options)

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8
Q

How many types of antigen recognition receptors does a single lymphocyte clone have?

A

Just one type, but it’s highly sensitive to that antigen

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9
Q

What are some cells of innate immunity?

A

Macrophages/monocytes, neutrophils, mast cells, NK cells, immature dendritic cells (before they become APC’s), innate lymphoid cells

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10
Q

What are some molecules of the innate immune system?

A

Complement system, natural autoantibodies, other soluble antimicrobial molecules (like defensins)

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11
Q

What are the two components of adaptive immunity?

A
  1. Cellular (as in T and B cells, APC’s are a link between adaptive and innate)
  2. Humoral: antibodies
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12
Q

At about what species in the evolutionary hierarchy do animals start obtaining an acquired immune system?

A

Sharks and some other fish, and everything more complex (reptiles, birds, mammals etc). It’s less universal than innate immunity, which are in all multicellular organisms.

Seems stupid but saw similar question on past papers

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13
Q

What type of antibodies are plasma cells NOT able to secrete?

A

IgD

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14
Q

What are the primary vs secondary immune organs?

A

Primary: (central) - where B and T cells are produced/mature, being the bone marrow and thymus

Secondary: (peripheral) - site of antigen encounter and activation of lymphocytes, meaning the lymph nodes, spleen, MALT, and SIS (skin immune system)

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15
Q

What happens if a recirculating lymphocyte recognizes an antigen in the secondary lymphatic organ?

A

It stops migrating, gets activated, and starts proliferating/dividing

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16
Q

What are the 3 phases of an immune response?

A
  1. Recognition Phase: activation, transformation
  2. Central Phase: clonal proliferation and differentiation
  3. Effector Phase: begins destroying/eliminating pathogens
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17
Q

What is the difference in time and amplitude between primary and secondary immune responses?

A

Primary immune response is slower to respond (longer latency) and has a lower amplitude response, due to having no memory cells to work with.

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18
Q

How many kDa are cytokines?

A

They’re small, <40 kDa (proteins usually ~ 53 kDa).

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19
Q

What are 4 shared features of cytokines? (i hate this kind of question too, sorry)

A
  1. exert functions via membrane receptors (high affinity, low number)
  2. effect is usually transitional (short halflife)
  3. functional redundancy
  4. antagonistic, additive, synergistic effects
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20
Q

What major histological differences do you see between resting lymphocytes and activated B or T cells?

A

Resting lymphocytes are smaller, their nucleus takes up most of their space. Activated ones are larger and they have a lot more rER for protein synthesis

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21
Q

When you deviate more and more from immunological homeostasis, what are 2 stages between homeostasis and inflammation?

A

Homeostasis -> stress response -> para-inflammation -> inflammation

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22
Q

How long does it take for adaptive immunity to develop in response to an infection?

A

7-14 days

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23
Q

Note: remember that graph showing if you lacked innate vs adaptive immunity, with Y axis being number of microorganisms and X axis being duration of infection

A

Either way you quickly die from infection, but the number of microorganisms increases much faster without innate immunity than acquired (logically)

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24
Q

How long does it take for innate immunity to act? And the early induced response?

A

Innate: 0-4 hours (immediately)

Early induced response: 4-96 hours

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25
Q

What are 3 types of barriers involved in the innate immune system?

A
  1. Mechanical: skin, mucous membrane, eyelid reflexes, etc
  2. Biological: normal bacterial flora, salivary and sweat enzymes, maternal antibodies, natural IgM
  3. Chemical: lower stomach and skin pH, ROS, NO, sebum..
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26
Q

Generally, what is the complement system?

A

System of serine proteases present in their inactive form all over the body, that, when activated, cleave and activate other complement proteins in a cascade manner. They help opsonize and lyse pathogens, as well as recruit inflammatory cells

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27
Q

What are natural autoantibodies?

A

Antibodies that are formed without any initial antigen exposure. They are low affinity and cross-reactive, they can recognize things like free viruses. May be IgM or IgA, and produced by B1 cells.

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28
Q

What are defensins?

A

Antimicrobial peptides that are amphipathic, with one positively-charged side chains and a hydrophobic side chain, allowing them to sink into membranes of bacteria/fungi and cause “wormholes.” They are part of the innate immune system, present all over the body - especially saliva.

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29
Q

Where is lysozyme present and what does it do?

A

Lysozyme is in the saliva, tears, and sweat. It cleaves a sugar moiety off peptidoglycans, which can degrade both Gram + and - bacterial cell walls

30
Q

What enzyme in saliva helps oxidize bacteria with H2O2?

A

Lactoperoxidase

31
Q

When monocytes are settled in connective tissue, what are they called?

A

Histiocytes

32
Q

How and to where do mature dendritic cells carry the antigen they found in the periphery?

A

They travel through the lymph vessels to a lymph node, and present antigens to T cells in the cortex.

33
Q

What are the 3 classes of human dendritic cells? (note: 1 of them has 2 subclasses)

A
  1. Myeloid: conventional dendritic cells. two subclasses: CDC1, which is 50% of all dendritic cells. CDC2: only 5-10% of all cells
  2. Plasmocytoid (pDC): 45-50% of all dendritic cells. Resembles plasma cells
  3. Monocyte-derived DC: small percentage of total DC’s. Involved in 2ndary immune response.
34
Q

What is responsible for the classical activation of recruited (non-resident) macrophages (M1)? What is the effect?

A

IFN-gamma -> M1 macrophage activation.

Effects: pro-inflammatory cytokines, bactericidal, anti-tumor

35
Q

What is responsible for the alternative activation of recruited macrophages (M2)? What is the effect?

A

IL-4 and IL-13 -> M2 macrophage activation. Vitamin D3 helps too (VitD3 may be anti-inflammatory)

Effects: removal of tissue/wound healing, anti-inflammatory (suppress T cell response and other defenses)

36
Q

What 3 kinds of signals are related to macrophage ingestion of apoptotic cells?

A
  1. “Find Me” - apoptotic cells attract macrophages with IL-8, MCP-1
  2. “Eat Me” - signal via phosphatidyl serine on apoptotic cell membrane
  3. “Tolerate Me” - after an apoptotic cell or fragment is ingested, immune response suppressed via anti-inflammatory cytokines like IL-10, TGF-beta, PGE2 (prevents other macrophages from being activated)
37
Q

What is it called when a phagocyte eats something coated in antibodies?

A

FcReceptor-mediated Phagocytosis. Uses a “zipper mechanism”

There is one for each type of antibody, i.e. Fc-Gamma Receptor for IgG, FcEpsilon receptor for IgE, etc.

(phagocyte could also use a complement receptor to do this)

38
Q

What is the unique type of Fc receptor that may suppress function of B cells?

A

Fc-Gamma Receptor IIb

39
Q

What is used to cleave the Fab from Fc region of antibodies?

A

Papain

40
Q

What is “frustrated phagocytosis?”

A

A phagocyte tries to eat something, but cannot (maybe it’s too big) - so the phagocyte dumps its lysozome contents on the pathogen surface in the EC space.

41
Q

Where are high-affinity Fc-Epsilon Receptors?

A

Mast cells and Basophils (IgE involved in allergy)

42
Q

Where is the FcRn receptor?

A

It’s the neonatal Fc receptor, binds IgG and helps transfer passive humoral immunity from mother to fetus. Protects IgG from degradation as they travel from maternal blood or breast milk to fetus/neonate.

43
Q

Where is the polyIg receptor?

A

In mucous membrane epithelium. Binds polymeric antibodies (IgA) and helps them cross from the basolateral side (where they were produced) to the apical side and be released on the surface.

44
Q

How does peroxidase-independent intravesical killing work?

A

O2 loses an electron via NADPH oxidase, that O2- goes on to from H2O2 that oxidizes pathogen

45
Q

What type of cell does myeloperoxidase act in?

A

Neutrophils, taking part in peroxidase-dependent intravesical killing

46
Q

How does the nitric oxide pathway in intravesical killing work?

A

IFNgamma induces NO synthase -> NOS with tetrahydrobiopterin -> O2 and arginine react to release NO and citrulline.

NOS with tetrahydrobiopterin can also be stimulated by TNF

47
Q

What does pus consist of?

A

Live and dead neutrophils and tissue debris. It kills the infection

48
Q

What disease does phagocyte oxidase deficiency cause?

A

CGD: Chronic Granulomatosis Disease

It’s a rare example of a disease impacting the innate immune system, which is usually not compatible with life

49
Q

How do Natural Killer cells work?

A

They’re from the lymphocyte lineage, but function differently, have no T or B cell receptor. They search for an MHC-I receptor, and kill anything without it. They use granzymes and perforins for their killing mechanism

50
Q

What are the activating and inhibiting NK cell receptors?

A

NKG2A: inhibitory receptor.

NKG2D: activating receptor.

NK cell activity is based on balance between the two. Ligands are the HLA molecules

51
Q

What are some functions of gamma delta T cells?

A

It’s an area of new research, they have a unique TCR. Involved in lysis of infected or stressed cells, dendritic cell maturation, B cell help and IgE production, etc.
(I don’t know what to say about this bc the details are vague, they aren’t really classifiable until more research is done. maybe more on the immunosupressive side)

52
Q

What are the 3 types of innate lymphoid cells (ILC)?

A

Type I: IFN gamma producers (NK cells)

Type II: producers of Th2 cytokines

Type III: secrete IL17 or IL22

53
Q

What are ILC’s?

A

New Research. Innate Lymphoid Cells: T cell subsets and allies to immune system. Very effective early defense. Characterized by plasticity, can transform to different types of cells.

54
Q

What are the 3 types of PRRs? (pattern-recognition receptor)

A
  1. Membrane PRRs
  2. Secreted PRRs
  3. Intracellular PRRs
55
Q

What are some membrane PRRs? (there are 5 listed)

Note that macrophages may have all of these types

A
  1. Lectin receptors (bind carbs like mannose)
  2. NK cell receptors
  3. Scavenger receptors
  4. Complement receptors
  5. Toll-like receptors (TLR)
56
Q

What is the effect of TLR binding to ligand?

A

MyD88 adaptor binding -> Ser/Thr kinase cascade -> phosphorylation of IkB -> (most importantly) NFkB translocation to nucleus -> expression of costimulatory molecules/cytokines (like IL-1) and MHC on the surface. Become efficient antigen-presenting cells

57
Q

What do TLR1 and TLR2 or TLR2 and TLR6 bind to?

A

Bacterial lipopeptides

58
Q

What does TLR2 bind to?

A

Bacterial peptidoglycans

59
Q

What does TLR4 bind to?

A

LPS

60
Q

What does TLR5 bind to?

A

Bacterial flagellin

61
Q

What does TLR3 (intracellular) bind to?

A

dsRNA

remember which TLR’s are intracellular: 3, 7, 8, 9

62
Q

What does TLR7 and TLR8 (intracellular) bind to?

A

ssRNA

63
Q

What does TLR9 (intracellular) bind to?

A

CpG DNA

64
Q

What are some examples of secreted pattern recognition receptors?
(again this shit is obnoxious and I don’t want to create a card for each one, just try to be familiar)

A

Antimicrobial peptides (i.e. defensins), pentraxins (i.e. C-reactive protein), C type lectins (Clq, MBL), cathelicidines, cationic peptides

(also listed: mindin, lipocalin, lipid transporter proteins)

65
Q

What’s an example of a cytosolic receptor that targets bacteria?

A

Nod-like receptor (NLR) - binds bacterial PAMPs that have made it into the cell

Has nucleotide binding domain and leucine-rich repeat binding proteins

66
Q

What’s an intracellular PRR that can detect viruses?

A

RIG-I-like receptor (RLR): detects helicase domain, cytoplasmic dsRNA

67
Q

What’s a DAMP?

A

Damage Associated Molecular Pattern - something associated with dying/necrotic cell. Binds to DAMP receptor of innate immune cell and stimulates pro-inflammatory response. Apoptotic cells hide these signals.

68
Q

What are 3 things that make up an inflammasome?

A

Caspace-1, NLR, and ASC adapter protein

69
Q

What is an inflammosome?

A

Cytoplasmic multiprotein oligomer which activates IL-1 beta and IL-18. These leave cell and are best-known inflammatory cytokines. (IL-33 included too, fuck I hate this)

70
Q

In the gut epithelium, why are there TLR’s intracellularly and on the basolateral surface, but not on the apical surface?

A

To allow intestinal flora to exist, and only attack them when they get inside or cross over

71
Q

What are autoinflammatory disorders?

A

Diseases with common feature of increased IL-1 beta secretion, causing the autoinflammation. Includes diseases like type 2 diabetes, familial mediterranean fever, gout, some types of arthritis, etc.

Immunology (By: Ben + Dustin) (12 decks)

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