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HDM > Midterm Exam Week 1 > Flashcards

Midterm Exam Week 1 Flashcards

1
Q

Why do warm-blooded, long-lived mammals have complex immune defenses?

A

Infectious agents such as bacteria thrive and can divide rapidly in warm-blooded creatures.

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2
Q

What is the role of commensal microflora in host defense mechanisms?

A

Microflora provide molecular signals for immune system development in each person.

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3
Q

Lactobacillus acidophilus

A

Major component of vaginal microflora
Metabolism of glycogen by L. acidophilus creates a vaginal pH of 5, resulting in the prevention of yeast colonization (which can often cause vaginitis- an inflammation of the vagina that can result in discharge, itching, and pain)

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4
Q

Vaginitis

A

inflammation of the vagina that can result in discharge, itching, and pain

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5
Q

Eye is protected against infections by which of the following?

a. the mucous membranes that cover their surface
b. the secretion of complement proteins
c. the release of slightly acidic secretions
d. the secretion of lysozyme onto their surface
e. interferons produced by immune cells

A

lysozyme (innate immunity)

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6
Q

Which statement about the complement system is true?

a. These proteins are involved in innate immunity and not acquired immunity.
b. These proteins are secreted by cytotoxic T cells and other CD8 cells.
c. This group of proteins includes interferons and interleukins.
d. These proteins are one group of antimicrobial proteins acting together in cascade fashion.
e. These proteins act individually to attack and lyse microbes.

A

antimicrobial cascade
Different initations:
1. Alternative- innate
2. Classical- adaptive
3. Leptin- innate (same as classical but no Ab)
Same efffects: C3a/C5a- inflammation
1. opsonization (C3b) and phagocytosis
2. leukocyte recruitment- neutrophils, monocytes (C3a, C5a)
3. MAC (polymeric protein complex)- microbe lysis

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7
Q

Which cells and which signaling molecules are responsible for initiating an inflammatory response?

a. phagocytes: lysozymes
b. phagocytes: chemokines
c. dendritic cells: interferons
d. mast cells: histamines
e. lymphocytes: interferons

A

mast cells: histamines
Mast cells are in most tissues, particularly in close contact with the external environment (skin, airways, and intestine) for early pathogen recognition
Within seconds of stimulation, mast cells can undergo degranulation, rapidly releasing pre‐formed mediators from cytoplasmic granules, including histamine

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8
Q

Inflammatory responses may include which of the following?

a. clotting proteins migrating away from the site of infection
b. increased activity of phagocytes in an inflamed area
c. reduced permeability of blood vessels to conserve plasma
d. release of substances to decrease the blood supply to an inflamed area
e. inhibiting the release of white blood cells from bone marrow

A

Inflammation includes

  • inc phagocyte activity (neutrophils, monocytes)
  • inc vessel permeability (leukocyte diapedesis/migration to tissue)
  • inc blood supply to inc imm response
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9
Q

Which of the following is most likely to be recognized by a particular TLR that defends against some viruses?

a. lipopolysaccharides
b. double‐stranded DNA
c. double‐stranded RNA
d. glycoproteins
e. phospholipids

A

TLRs are key feature of innate immunity: pattern recognition receptors (PRRs) for PAMPs
Recognized PAMPs include
-LTA (gram pos bacteria)
-LPS (gram neg bacteria)
-flagellin (bacteria)
-ssRNA and dsRNA (viruses)
PAMP recognition activates signaling pathways and induces production of cytokines and chemokines

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10
Q

Histamines trigger dilation of nearby blood vessels, and increase in their permeability. Which of the signs of inflammation are therefore associated with histamine release?

a. redness and heat only
b. swelling only
c. pain
d. redness, heat, and swelling
e. all of the signs of inflammation

A 
4 Cardinal Signs of Inflammation: 
   1. Calor (heat)
   2. Dolor (pain)
   3. Rubor (redness)
   4. Tumor (swelling)
Histamines trigger THREE
Dilation-> more warm blood-> heat/redness
More permeability-> more fluid leakage-> swelling
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11
Q

One reason that pathogenic microorganisms have an advantage in the host they infect is because they:

a. have previously been encountered through natural exposure
b. have previously been encountered through vaccination
c. strengthen the host’s immune response
d. reproduce and evolve more rapidly than the host can eliminate them
e. reproduce and evolve more slowly than the host can eliminate them.

A

Pathogenic microorganisms reproduce and evolve more rapidly than the host can eliminate them

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12
Q

Which of the following is not a characteristic of inflammation?

a. inactivation of macrophages
b. increased vascular permeability and edema
c. vasodilation
d. pain
e. influx of leukocytes.

A

4 Cardinal Signs of Inflammation
1. Calor (heat)
2. Dolor (pain)
3. Rubor (redness)
4. Tumor (swelling)
Inflammation-> neutrophils die-> release contents and form NETs
Inflammation is associated w/leukocyte recruitment (IL8), vasodilation, vessel permeability
Macrophages produce cytokines that initiate/regulate inflammation

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13
Q

Which of the following pairs is mismatched?

a. lymphocytes: innate immune response
b. natural killer cell: kills virus‐infected cells
c. macrophage: phagocytosis and killing of microorganisms
d. erythrocyte: oxygen transport
e. eosinophil: defense against parasites.

A

Lymphocytes are part of adaptive immunity (B and T cells), although NK cells are innate.
NK cells kill virus-infected cells and phagocytosed microbes.
Macrophages phagocytose and kill microorganisms when classically activated (innate immunity). Alternative activation allows macrophages to control inflammation and repair tissues/inc fibrosis (adaptive immunity).
RBCs are the only cells without MHC I; however, NK cells do not kill them because NK cells are in tissues, NOT circulation.
Eosinophils are associated w/IL5 and help defend against extracellular parasites (helminths)

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14
Q

Examples of granulocytes include all of the following except:

a. neutrophil
b. monocyte
c. basophil
d. eosinophil.
e. All of the above are examples of granulocytes.

A 
FOR MY MEMORY: MEB'N
Mast cells
Eosinophils
Basophils
Neutrophils

Monocytes/macrophages are not granulocytes.

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15
Q

The most abundant type of leukocyte in human peripheral blood is:

a. eosinophil
b. basophil
c. neutrophil
d. monocyte
e. lymphocyte.

A

Neutrophils, fundamental to INNATE immunity
Low levels inc risk of bact/fung infection
-neutropenia
-chronic granulomatous disease (NADPH oxidase defect-> ineffective phagolysosome)
-leukocyte adhesion deficiency syndrome (LFA-1 defect, impaired stabilization of T cells binding to ICAM-1 on APCs, umbilical cord sep. delay)

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16
Q

Koch’s Postulates

A
  1. Infected tissue shows presence of microorganisms not in healthy tissue
  2. Microorganism isolated, grown in pure culture
  3. Injected in healthy tissue/animal, causes disease
  4. Microorganism isolated, shown to be identical to 1
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17
Q

Gram-positive bacterial wall structure

A

Stains purple
thick peptidoglycan layer
Lipoteichoic acid (recognized by TLR2:6)
TLR1,2,6 recognizes LPS for G+

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18
Q

Gram-negative bacterial wall structure

A

Stains pink
thin peptidoglycan layer
LPS (recognized by TLR4:4)

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19
Q

Host defense mechanism for extracellular pathogens

A

NK cells, T cells- perforin
Complement- MAC
Neutrophils, Macrophages- phagocytosis
Granulocytes- degranulation

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20
Q

Host defense mechanism for intracellular pathogens

A

only eliminated by cellular immune response, NO ABS

tissue damage caused by inflammation (ex- tuberculosis)

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21
Q

Germ-free animals

A

C-section

don’t have any commensal microflora

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22
Q

Intracellular Bacteria

A

shielded from Abs
disease mechanism due to host immune response
Ex: Mycobacterium tuberculosis, Legionella pneumophila

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23
Q

Extracellular Bacteria

A

Replicate outside host cells (circulation, conn tissue, airways, GI tract)
Induce inflammation (resulting in tissue destruction) and produce toxins (endotoxin from cell wall, secreted exotoxins)
Ex: staphylococcus aureus, Clostridium tetani, Neisseria meningitidis, Escherichia coli

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24
Q

Immune System Components

A

Fixed Elements (lymphoid organs)
Primary: bone marrow, thymus
Secondary: spleen/lymph nodes, mucosal immune tissues
Mobile Elements
Immune cells
Soluble/humoral components: antibodies, complement, acute phase proteins, etc.

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25
Q

Immune cells in blood

A 
RBCs
Platelets
Leukocytes
   Granulocytes/Polymorphs
      Eosinophil
      Basophil
      Phagocyte: Neutrophil
   Mononuclear cells
      Lymphocytes: T cell, B cell, NK cell
      Phagocyte: Monocyte
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26
Q

Immune cells in tissue

A 
Tissue eosinophil
Mast cell (basophil in blood)
Macrophage/histocyte (monocyte in blood)
T lymphocyte (T cell in blood)
Plasma cell (B cell in blood)
NK cell
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27
Q

Functional Classification of Lymphoid Tissue

A

Primary Lymphoid Organs: produce cellular components
- Thymus & Bone marrow
Secondary Lymphoid Organs: where immune responses occur
- Spleen, Tonsils, Lymph nodes

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28
Q

Capsular Classification of Lymphoid Tissue

A
  • Non-Encapsulated
    • Diffuse
    • Nodular
      • Single
        • Primary Nodule
      • Secondary Nodule
        • Aggregate
          • Tonsils
            • Pharyngeal
            • Palatine
            • Lingual
          • Peyer’s Patches
          • Vermiform Appendix
  • Capsulated
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29
Q

Non-encapsulated lymphoid tissue

A
  • Diffuse
  • Nodular
    • Single: lymphocytes
      • Primary Nodule
      • Secondary Nodule (germ center + mantle)
    • Aggregate
      • Tonsils
        • Pharyngeal (Partial)
        • Palatine (Partial)
        • Lingual (Undefined)
      • Peyer’s Patches (GALT, villi)
      • Vermiform Appendix (GALT, crypts)
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30
Q

Non-encapsulated lymphoid tissue: nodular (vs diffuse)

A
  • Single: lymphocytes
    - Primary Nodule
    - Secondary Nodule (germ center + mantle)
    • Aggregate
      • Tonsils
        • Pharyngeal (Partial)
        • Palatine (Partial)
        • Lingual (Undefined)
      • Peyer’s Patches (GALT, villi)
      • Vermiform Appendix (GALT, crypts)
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31
Q

Non-encapsulated lymphoid tissue: aggregate (vs single- primary/secondary)

A
  • Tonsils
    - Pharyngeal (Partial)
    - Palatine (Partial)
    - Lingual (Undefined)
    - Peyer’s Patches (GALT, villi)
    - Vermiform Appendix (GALT, crypts)
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32
Q

Adaptive immunity

A

improves on repeated exposure to given infection (memory)

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33
Q

Opsonin

A

Small fragment in the complement system

Deposited on microbes to enhance uptake by phagocytes bearing complement receptors

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34
Q

Antibody

A

Secreted by plasma cells in adaptive immunity
part of BCR on B-cells
Made of identical heavy and light chains
Immunoglobulin family, class switching maintains antigen specificity (Fab) but changes effector cell (Fc)
Papain generates 2 Fab fragments

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35
Q

Cytokine

A

Small protein secreted by many types of cells
Mediate inflammation, immunity, hematopoiesis
Endocrine, paracrine, or autocrine
Includes interleukins and interferons, chemokines, TNF

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36
Q

Cytokines (innate immunity)

A

Pro-inflammatory
Anti-inflammatory
Work together (at some point you have to stop an inflammatory response through apoptosis/macrophages)
Macrophages activate all except IFN-gamma (which activate them instead)
Examples: TNF, IL-1, chemokines, IL-12, IFN-gamma, IFN-alpha/beta (Type I), IL-10, IL-6, IL-15, IL-18
FUNCTIONS OF EACH

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37
Q

Complement system

A

Consists of a set of serum proteins that normally exist as soluble inactive precursors
Activation pathways: CLASSIC, ALTERNATIVE, LECTIN
Cleave precursors-> large and small fragments
Large fragments- enzymatic, activate formation of Membrane Attack Complexes (MACs)-> disrupt pathogen membranes
Small fragments- opsonins, chemotactic factors, anaphylatoxins
2 Phases
1. C3 activated: C3-> C3b-> C3a- inflammation -> C3b (deposited on microbe)- opsonization/phagocytosis
2. C5 activated: C5-> C5b-> C5a- inflammation -> C9- membrane pore formation (by MAC) -> lysis of microbe

38
Q

PAMP

A

Pathogen-associated molecular pattern

39
Q

Pattern Recognition Receptors

A

Cell receptors recognizing PAMPs

40
Q

TLR1:TLR2 heterodimer (receptor)

A

Ligands: lipopeptides, GPI
Microorganisms recognized: bacteria, parasites (ex- trypanosomes)
Cells carrying receptor: monocytes, dendritic cells, eosinophils, basophils/mast cells
Cellular location of receptor: plasma membrane

41
Q

TLR2:TLR6 heterodimer (receptor)

A

Ligands: lipoteichoic acid, zymosan
Microorganisms recognized:gram-POS bacteria, yeasts/fungi
Cells carrying receptor: monocytes, dendritic cells, eosinophils, basophils/mast cells
Cellular location of receptor: plasma membrane

42
Q

TLR3 (receptor)

A

Ligands: double stranded viral RNA
Microorganisms recognized: viruses (ex- West Nile virus)
Cells carrying receptor: NK cells
Cellular location of receptor: Endosomes

43
Q

TLR4:TLR4 homodimer (receptor)

A

Ligands: lipopolysaccharide (LPS)
Microorganisms recognized: gram-NEG bacteria
Cells carrying receptor: macrophages, dendritic cells, mast cells, eosinophils
Cellular location of receptor: plasma membrane

44
Q

TLR5 (receptor)

A

Ligands: flagellin
Microorganisms recognized: motile bacteria w/flagellum
Cells carrying receptor: intestinal epithelium
Cellular location of receptor: plasma membrane

45
Q

TLR7 (receptor)

A

Ligands: single-stranded viral RNAs
Microorganisms recognized: viruses (ex- HIV)
Cells carrying receptor: plasmacytoid dendritic cells, NK cells, eosinophils, B cells
Cellular location of receptor: endosomes

46
Q

TLR8 (receptor)

A

Ligands: single-stranded viral RNAs
Microorganisms recognized: viruses (ex- influenza)
Cells carrying receptor: NK cells
Cellular location of receptor: endosomes

47
Q

TLR9 (receptor)

A

Ligands: unmethylated CpG-rich DNA
Microorganisms recognized: bacteria, viruses (ex- herpes viruses)
Cells carrying receptor: plasmacytoid dendritic cells, B cells, eosinophils, basophils
Cellular location of receptor: endosomes

48
Q

TLR10 homodimer, TLR10:TLR1 heterodimer, TLR10:TLR2 heterodimer

A

Ligands: unknown
Microorganisms recognized: unknown
Cells carrying receptor: plasmacytoid dendritic cells, basophils, eosinophils, B cells
Cellular location of receptor: unknown

49
Q

Phagolysosome

A

Phagosome (contains substrate) fuses with lysosome (contains enzymes)
Enzymes: Phagocyte oxidase (creates Reactive Oxygen Species), inducible Nitric Oxide Synthase (creates NO)

50
Q

Chronic Granulomatous Disease

A

Genetic disorder caused by a defect in NADPH oxidase activity and inability to produce H2O2
Leads to chronic and recurrent bacterial infections

51
Q

Chemokine

A

Small protein chemoattractants for trafficking immune cells

52
Q

Chemotactic factors

A

Small fragments in the complement system

Attract immune cells

53
Q

Anaphylatoxins

A

Small fragments in the complement system
Cause degranulation of mast cells/basophils
Release vasoactive substances

54
Q

Classic pathway

A

Most sensitive complement activation pathway

Activated by antigen-antibody complexes (Ag-Ab)

55
Q

Alternative pathway

A

Least sensitive complement activation pathway

Activated by microbial cell walls

56
Q

Lectin pathway

A

Complement activation pathway (sensitivity b/w classic and alternative)
Interaction of microbial carbohydrates w/mannose-binding protein in the plasma

57
Q

Large fragments

A

Product of the complement system (precursors cleaved to large and small fragments)

Enzymatic fragments

Phase 2 of complement system: C5 activates formation of lytic sequence/Membrane Attack Complexes (MACs)-> disrupt pathogen membranes

58
Q

Small fragments

A

Product of the complement system (precursors cleaved to large and small fragments)

Opsonins, chemotactic factors, anaphylatoxins

Phase 1 of complement system: C3 activates inflammation, opsonization, and phagocytosis

59
Q

A workup on an ill child revealed low levels of complement C3 in her blood. Which one of the following presentations did this child most likely manifest?

A. Chronic eczema
B. Immune hemolytic anemia
C. Incomplete recovery from viral infections
D. Poor response to vaccination
E. Recurrent infections w/extracellular bacteria

A

E

60
Q

Nails

A

Keratinized plates of cells on bed of epidermis (analogous to stratum corneum)
Nail plate on nail bed
Nail matrix at bottom of plate, Lunula is white area just above
Eponychium= cuticle (fold of stratum corneum)
Hyponychium under distal nail plate (fold of stratum corneum)

61
Q

Lymphoid System

A

Functional classification: primary and secondary lymphoid organs
Capsular classification: non-encapsulated and capsulated
Lobules (thymus) v No Lobules (spleen, lymph nodes)

62
Q

Leukocyte Adhesion Deficiency

A

Defect in lymphocyte function-associated Antigen 1 (LFA-1)
Manifests by recurrent bacterial infections, defects in neutrophil chemotaxis (inability to form pus), and a delay in umbilical cord separation
LFA-1 is a T cell integrin that helps stabilize binding to APC ICAM-1

63
Q

Ig A deficiency

A

defect in production of IgA
patients should be evaluated through comprehensive stool analysis for hidden GI infections (parasites, candida, bacteria)

64
Q

Ig class switching

A 
B cell switches production of immunoglobulins
Fab stays same (binds same antigen)
Fc changes (interacts w/DIFF effector cell)
65
Q

TLR 1:2 heterodimer

A

PRR that recognizes lipopeptides (bact) and glycoprotein 1 (parasites)
FOR MY MEMORY: heterodimer=recognizes 2 things, 1 for GP1 (p for parasites)
Present in plasma membrane of monocytes, dendritic cells, eosinophils, and basophils/mast cells

66
Q

TLR 2:6 heterodimer

A

PRR that recognizes LTA (G+ bact) and zymosan (yeast/fungi)
FOR MY MEMORY: heterodimer=recognizes 2 things, 6/2=3 (G+ bact, yeast, fungi)
Present in plasma membrane of monocytes, dendritic cells, eosinophils, and basophils/mast cells

67
Q

TLR 3

A

PRR that recognizes viral dsRNA

Present in endosomes of NK cells

68
Q

TLR 4:4 homodimer

A

PRR that recognizes LPS (G- bact)

Present in plasma membrane of macrophages, dendritic cells, eosinophils, and mast cells

69
Q

TLR 5

A

PRR that recognizes flagellin (motile bacteria)

Present in plasma membrane of intestinal epithelial cells

70
Q

TLR 7

A

PRR that recognizes viral ssRNA (ex- HIV)
FOR MY MEMORY: seven starts w/S & has a V in it
Present in endosomes of NK cells, dendritic cells, eosinophils, B cells

71
Q

TLR 8

A

PRR that recognizes viral ssRNA (influenza)
FOR MY MEMORY: 8=ocho-> Spanish flu-> influenza
Present in endosomes of NK cells

72
Q

TLR 9

A

PRR that recognizes unmethylated CpG-rich DNA (herpes)
FOR MY MEMORY: complicated snake in the shape of the number 9
Present in endosomes of dendritic cells, eosinophils, basophils, B cells

73
Q

TLR 10:10 homodimer

TLR 10:1, 10:2 heterodimers

A

PRR that has unknown ligand

Present in endosomes of dendritic cells, eosinophils, basophils, B cells

74
Q

What is the most abundant antibody isotope in the body?

A

IgA
Dimeric
GI tract lumen (only innate/humoral immunity here because no blood flow)

75
Q

What is the most abundant antibody isotype in the blood?

A

IgG
Monomeric
Starts complement system

76
Q

What antibody isotype is only found in the blood?

A

IgM (pentamer)
B cell receptor
Starts complement system
Involved in allergic reactions and other things

77
Q

What HLA genes are associated with MHC I?

A

HLA-A, B, C

78
Q

What HLA genes are associated with MHC II?

A

HLA-DP, DQ, DR

79
Q

Which antibody isotype is always on the membrane?

A

IgD
B cell receptor
Never cleaved off to do other things in the blood

80
Q

Which cell is the first to the infection site?

A

Neutrophils
Innate immune response
Replaced by marophages in a few days

81
Q

Mycobacterium tuberculosis

A

Intracellular bacteria
Disease: tuberculosis, leprosy
Macrophage activation-> granulomatous inflammation + tissue destruction

82
Q

Legionella pneumophila

A

Intracellular bacteria
Disease: Legionnaires’ disease
Cytotoxin lyses cells and causes lung injury + inflammation

83
Q

Staphylococcus aureus

A

Extracellular bacteria
Disease: skin/soft tissue infections, lung abscess, toxic shock syndrome, food poisoning
Mechanism: enterotoxin-induced inflammation and cytokine release -> skin necrosis, shock, diarrhea

84
Q

Clostridium tetani

A

Extracellular bacteria
Disease: tetanus
Mechanism: tetanus toxin-> irreversible muscle contraction

85
Q

Neisseria meningitidis

A

Extracellular bacteria
Disease: meningitis
Mechanism: potent endotoxin (LPS)-> acute inflammation and systemic disease

86
Q

Escherichia coli

A

Extracellular bacteria
Disease: UTIs, gastroenteritis, septic shock
Mechanism: toxins-> inc chloride/water secretion; endotoxin (LPS)-> cytokine secretion by macrophages

87
Q

innate immunity

A

occurs to same extent every time infectious agent is encountered

88
Q

Neutrophils

A

Main function: phagocytosis
make cytokines/prostaglandins, degranulation, form NETs
Granules: lysozyme, lactoferrin, PLA2, peroxidase, elastase, etc.
attracted by IL8

89
Q

Lactoferrin

A

binds iron to make unavailable to bacteria

90
Q

Monocytes

A

Become macrophages in tissue
Main function: Phagocytosis
Make cytokines, ROI, NO, defensins, lipases, galactosidase

91
Q

Macrophages

A

APCs
Produce IL12, TNF for T helper response (which makes IFN gamma and returns stimulation)
Involved in many autoimmune and inflammatory diseases (TNF and IL1)
Keloid scars caused by overactivation

HDM (6 decks)

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