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Physiology (MPP 3202) > Ch. 15 Immunology > Flashcards

Ch. 15 Immunology Flashcards

1
Q

What are the physical barriers of the immune system?

A

Skin and mucosal membrane

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2
Q

Name the 4 infectious pathogens.

A

Parasites
Fungi
Bacteria
Viruses

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3
Q

Innate immune response

A

Nonspecific

Includes external and internal defenses, including inflammatory response

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4
Q

Adaptive immune response

A

Acquired, specific, learned

Ability to form immune “memory” from previous exposure

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5
Q

Function of immune system?

A

Defense against damaging molecules and foreign invaders

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6
Q

Primary lymphoid tissues

A

Thymus gland and bone marrow

Formation and maturation of immune cells

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7
Q

Secondary lymphoid tissues

A

Tonsils, lymph nodes in body, spleen

Interaction of mature immune cells with pathogens and initiation of immune responses

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8
Q

2 classes of cells in the immune system?

A

Adaptive

Innate

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9
Q

Adaptive cells

A

“Lymphocytes” (lymphoid stem cells)

B cells

  • plasma cells
  • memory cells

T cells

  • Th cell
  • Tc cell
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10
Q

Innate cells

A

“Granulocytes” (myeloid progenitor)

Natural killer cells

Neutrophil

Eosinophil

Basophil

Mast cell

Monocyte

  • dendritic cell
  • macrophage
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11
Q

Dendritic cells and macrophages are?

A

APCs (antigen presenting cells)

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12
Q

Macrophages are granulocyte and ____.

A

phagocytes

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13
Q

How are pathogens recognized?

A

Pathogen Associated Molecular Patterns (PAMP) recognized by Pattern Recognition Receptors (PRR) on the surface of macrophages

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14
Q

What is PAMP?

A

Pathogen Assoc. Molecular Patterns located on bacterium/foreign pathogen that a PRR on a macrophage will recognize

ex: LPS component of outer wall of G- bacteria (like E. coli)

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15
Q

What is PRR?

A

Pattern Recognition Receptors

Recognize PAMP; located on macrophages

Also located on most cells in body, but these notes are discussing macrophages

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16
Q

DAMPs

A

Danger/Damage Assoc. Molecule Patterns

PAMPs are just one type of DAMP

PRRs recognize molecules released by OUR own damaged or dying cells (DAMP)

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17
Q

Phagocytosis

A
  1. Macrophage comes into contact w/ pathogen
  2. Engulfment into phagosome
  3. Fusion w/ lysosomes
  4. Destruction
  5. Release of harmless molecules
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18
Q

Give a few examples of phagocytes and where they’re located in the body.

A
  1. Neutrophils (blood and all tissues)
  2. Monocytes (blood)
  3. Tissue macrophages (all tissues, including spleen, lymph nodes, bone marrow)
  4. Kupffer cells (liver)
  5. Alveolar macrophages (lungs)
  6. Microglia (CNS)
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19
Q

Macrophages have how many stages of activation?

A

3 stages of activation:

  • resting/quiescent
  • activated/primed
  • hyperactivated
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20
Q

Macrophage Activation: Resting/quiescent

A

Stage 1

Clean up debris/garbage from cell death/turnover [dying cells release DAMPs too]

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21
Q

Macrophage Activation: Activated or Primed

A

Stage 2

In response to cytokines (IFN-gamma), macrophages take bigger “gulps,” express MCH-2 molecules for “antigen presenting”

22
Q

Macrophage Activation: Hyperactivated

A

Stage 3

In response to DIRECT CONTACT with PAMPs (ex: LPS or mannose), becomes huge killing machine

Increase in:
-size, lysosomes, rate of phagocytosis, release of TNF, IL-1 (kill tumor cells, virus-infected cells, activates other immune cells) and oxidants (ex: H2O2)

23
Q

Inflammation

A

Innate immunity - nonspecific response

Movement of neutrophils is tightly restricted to specific sites of injury

24
Q

Circulating leukocytes interact with the vascular endothelium near the site of injury via specific molecular interactions with ____ ____.

A

Adhesion molecules

-these interactions are tightly regulated

25
Q

What are 3 soluble factors which promote inflammatory response?

A
  1. Acute phase proteins
  2. Complement
  3. Opsonin function
26
Q

Acute phase proteins

A

e.g. antibodies/other microbe binding proteins (opsonins), C-reactive protein; secreted by liver, circulate in plasma; some facilitate pathogen recognition by binding to “coated” bacteria, others are inhibitors of pathogen-secreted proteases

27
Q

Complement

A

Plasma and membrane proteins

act as opsonins, cytotoxins (membrane attack complex [MAC]), stimulators of inflammatory cells

28
Q

Opsonin function

A

An opsonin is a molecular “red flag’ which targets pathogens for attack/destruction

ex: antibodies, complement

29
Q

How do antibodies also “opsonize” (decorate) pathogens?

A

Tages pathogen for destruction - “kill/eat”

Serves as molecular bridge between invader and phagocytic cell

Engagement w/ Fc receptor triggers activation of macrophage

Can block viral entry/post-entry replication

30
Q

What are the 2 regions of an antibody?

A

Fc region

Variable region

31
Q

Antibody defense is ____ is virus gains entry to host cell.

A

inadequate

32
Q

Do plasma cells (subtype of B cell) have memory?

A

NO

33
Q

Antibodies

A

Immunity is conferred by antibodies - immunoglobulin (Ig) proteins produced and released by B-lymphocytes (plasma B cells) - a given B cell “clone” produces antibody against a single, specific antigen

Antibody diversity generated by mixing and matching of several different types of DNA segments –> molecular design
–can create over 100 million different possible combinations

34
Q

IgG composes __% of all antibodies

A

75%

35
Q

The __ ___ ____ is a cell surface-resident version of the antibody molecule.

A

B cell receptor

36
Q

____ region of the receptor linked by accessory proteins to signaling pathways which trigger B cell activation.

A

Cytoplasmic

37
Q

What determines whether a B cell becomes a plasma or memory cell?

A

The way it’s activated

–if there’s a second signal requiring a T cell, the B cell becomes a memory cell

38
Q

Memory cells require __ ____ dependent activation

A

T cell

39
Q

Effector cells are known as?

A

Plasma cells

40
Q

What are the 2 simultaneous signals B cell activation requires?

A
  1. clustering (“crosslinking”) of B cell receptors

2. binding to an activated helper T cell (T cell dependent activation) or by recognition of “danger molecules”

41
Q

T/F: T cell dependent activation is required for B cell –> memory cell.

A

true

42
Q

Acquired immunity and memory cells

A

Acquired immunity is specific, antibody dependent response

“memory cells” respond faster than naive cells - second exposure to antigen is faster and more robust than after first exposure
–this is why vaccines are useful

43
Q

T cells: similarities w/ B cells

A

Surface receptors (TCR [T cell receptor]) - antibody like

Like BCR (B cell receptor), TCR also results from modular construction via gene shuffling/recombination

Like B cells, T cells also undergo clonal selection in response to specific antigen recognition

44
Q

T cells: differences from B cells

A

B cells mature in bone marrow, T cells in thymus

BCR/antibody recognize any organic molecule, TCR recognize ONLY protein antigens

B cells can export (secrete) its BCR’s in form of antibodies, but TCR’s are restricted to surface of T cells

B cell can recognize an antigen “by itself” but T cells ONLY recognize antigens that are properly presented by another cell (antigen presenting)

45
Q

TCR Proteins

A

Antigen recognition dependent on “presentation”

Antigen recognition proteins on membranes of T cells:

  • 1) cannot bind directly to antigens
  • 2) APCs, such as dendritic cells and macrophages, help T cells bind to antigens by processing and presenting them
46
Q

Dendritic Cells

A

Originate in marrow and migrate to most tissue (esp. where pathogens might enter body)

Engulf protein antigens, partially digest them, and display polypeptide fragments on their surface for T cells to “see”

  • a) antigen fragments assoc. w/ histocompatibility antigens
  • b) secrete cytokines to attract T lymphocytes in secondary lymphoid organs

Once activated, T cells divide to form effector T cells and memory T cells

47
Q

What are the classes of MHC molecules?

A

Class 1

Class 2

48
Q

MHC molecules: Class 1

A

made by all cells except RBCs

Class 1 MHC molecules and foreign antigens presented together to activate cytotoxic T cells

Activate Killer T cells

49
Q

MHC molecules: Class 2

A

Made by APCs and B cells

Class 2 MHC molecules and foreign antigens presented TOGETHER to helper T lymphocytes

50
Q

Rule of 8s

A

Killer T cells have CD8 for MHC-1

Helper T cells have CD4 for MHC-2

51
Q

Viruses

A

undergo constant mutation and gene shuffling, so immune memory of a given infection is no guarantee against future infections
–this is why flu shot is a yearly thing

Viral surface antigens contain Hemagglutinin (H) and Neuraminidase (N)
–ex: H1N1 (common human “A” flu strain) and H5N1 (“bird flu”)

52
Q

How do viruses undergo mutations?

A

Occurs from antigenic shift (genetic shuffling) and antigenic drift (random mutation)

Physiology (MPP 3202) (32 decks)

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