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Allergy and Immunology > Innate and Adaptive Immunity > Flashcards

Innate and Adaptive Immunity Flashcards

1
Q

What are the steps for phagocyte mobilization?

A
  1. Leukocytosis ( release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells)
  2. Margination (neutrophils cling to the walls of capillaries in the inflamed area)
  3. Diapedesis of neutrophils
  4. Chemotaxis (inflammatory chemicals, chemotactic agent, promote postive chemotaxis of neutrophils)
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2
Q

What are the mechanisms buy which phagocytosis works to destroy pathogens? 3 ways

A
  1. Destruction of pathogens (acidification and digestion by lysosomal enzymes)
  2. Respiratory burst
  3. Oxidizing chemicals
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3
Q

What are the innate external defenses?

A

skin, mucous membranes and secretions, skin acidity, lipids in sebum, dermcidin in sweat, HCL in stomach, lysozyme in saliva, mucus, haris, cilia

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4
Q

What are the general innate internal defenses (cells and chemicals)? Meaning, what does the innate immune response do, what is it responsible for? As well as cells, and proteins.

A
  1. phagocytes
  2. NK
  3. Inflammatory response (macrophages, mast cells, WBC, inflammatory chemicals)
  4. Antimicrobial proteins (complement proteins and interferons)
  5. Fever
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5
Q

What are the functions and characteristics of NK cells?

A
  • large granular lymphocytes
  • target cells that lack “self” cell-surface receptors WITHOUT previous exposure to surface antigens
  • induce apoptosis in cancer cells and virus infected cells
  • secrete potent chemicals that enhance the inflammatory response
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6
Q

When is inflammation triggered? How does it help in the immune response?

A
  • triggered whenever body tissues are injured or infected
  • prevents the spread of damaging agents
  • disposes of cell debris and pathogens
  • sets stage for repair
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7
Q

cardinal signs of inflammation are?

A 
redness
swelling
heat
pain
immobility (sometimes)
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8
Q

What FIRST needs to happen to start the process of inflammation? (what promotes it, and what causes the that promotion to occur?)

A
  1. macrophages and epithelial cells of boundary tissues bear TLRs
  2. TLRs actviated trigger the release of cytokines
  3. Cytokines promote inflammation
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9
Q

What are the inflammatory mediators?

What are they released by?

A
  • –histamine (from mast cells), blood proteins, kinins, prostaglandins, leukotrienes and complement
  • –released by injured tissues, phagocytes, lymphocytes, basophils and mast cells
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10
Q

What do inflammatory chemicals cause?

A
  • dilation of arterioles, resulting in hyperemia

- increased permeability of local capillaries and edema =(leakage of exudate)

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11
Q

what is exudate? What does it contain?

A
  • -exudate is a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation
  • -contains proteins, clotting factors and antibodies
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12
Q

What is the function of exudate?

A
  • -moves foreign material into lymphatic vessels

- -delivers clotting proteins to form a scaffold for repair and to isolate the area (collagen and fibrin)

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13
Q

What are the steps of IFN production? Starting with virus entering cell.

A
  1. virus enters cell
  2. interferon gene inside cell turns on
  3. cell produces interferon molecules
  4. interferon is then secreted from that cell
  5. interferon enters neighboring cells–or binds to cell
  6. interferon stimulates cell to turn on genes for antiviral proteins
  7. antiviral proteins block viral reproduction in cell
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14
Q

What interferon do lymphocytes secrete?

A

gamma = immune interferon

p. 287 (also NK and macrophages)

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15
Q

What IFN do most WBCs secrete?

A

alpha

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16
Q

What IFN do fibroblasts secrete?

A

beta

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17
Q

What cells do IFNs activate?

A

macrophages and mobilize NK cells

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18
Q

What is the function of interferons?

A
  • antiviral
  • reduce inflammation
  • activate macrophages and mobilize NK cells
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19
Q

What do genetically engineered INFs do?

A
  • antiviral agent against hepatitis, genital warts

- MS treatment

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20
Q

What are the three phases of complement?

A
  1. Initiation or activation
  2. amplification of inflammation
  3. Membrane attack response (promotes phagocytosis and causes cell lysis)
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21
Q

What does C3a do?

A

triggers migration of neutrophils in the the tissues to enhance the inflammatory response

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22
Q

What does C3b do?

A

INITIATES the formation of a MAC and also opsinization

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23
Q

What does C5a do?

A

inflammation

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24
Q

What does MAC do?

A

cell lysis

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25
Q

What complement proteins are the mac made of?

A

C3b starts it, then C5b, C6, C7, C8, C9

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26
Q

What are the benefits of a moderate fever?

A
  • -causes liver and spleen to sequester iron and zinc

- -increases metabolic rate which speeds up healing

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27
Q

What happens to self reactive B cells?

A

they undergo clonal deletion
or
they undergo receptor editing (rearrangement of their receptors)

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28
Q

What is positive and negative selection in T cells?

A

First step= positive selection
T cells must recognize self MHC proteins or they will die
Called MHC restriction (survivors are restricted to recognizing antigen on self-MHC)
second step = negative selection
T cells MUST NOT recognize self-antigen or will die = autoimmune diseases!
failure to recongize (bind tightly to) self antigen results in SURVIVAL and continued maturation

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29
Q

What is an antigen?

A
  • substance that can mobilize the ADAPTIVE defense and provoke an immune response
  • -most are large, complex molecules not normally found in the body (non self)
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30
Q

What is a complete antigen? What is does it mean that it is immunogenic and reactive? What are some examples?

A

Immunogenicity = ability to stimulate proliferation of specific lymphocytes and antibodies
Reactivity = ability to react with products of activated lymphocytes and antibodies released
examples: foreign protein, polysaccharides, lipids, nucleic acids (bacteria and viruses)

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31
Q

What is a hapten?
What does the hapten do?
What are some examples?

A

hapten = small molecules (peptides, nucleotides, hormones)

  • -haptens are IMMUNOGENIC when attached to BODY PROTEINS
  • cause immune system to mount a HARMFUL attack
    ex. poison ivy, animal dander, detergents, cosmetics
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32
Q

What are the adaptive defenses?

A
  • -specific, systemic, has memory!
  • protects against infections agents and abnormal body cells
  • amplifies inflammatory response
  • activates complement
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33
Q

What is the humoral adaptive defense consist of and what is it mediated by and what does it defend against?

A

B-cells, antibodies, plasma cells

  • mediated by B-cell activation and subsequent Ab production
  • primary defense against EXTRAcellular microbes and toxins
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34
Q

What is the cell-mediated adaptive defense consist of and what is it mediated by and what does it defend against?

A

T-cells, Cytotoxic T-cells, Helper T-cells

  • -mediated by activation of T-cells
  • responsible for the bodies defenses against intracellular mnicrobes such as viruses
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35
Q

What molecule has little or no immunogenicity?

A

large, chemically simple molecules

plastics, valves, hips

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36
Q

What is an antigenic determinant?

A
  • certain part of antigen that is immunogenic
  • Ab and lymphocytes bind to them
  • most have numerous antigenic determinants that: 1. mobilize several different lymphocyte pops and 2. form different Ab against it
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37
Q

Finish the sentence. Most naturally occurring antigens have numerous antigenic determinants that:

A
  1. mobilize several different lymphocyte populations

2. form different kinds of antibodies against it

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38
Q

What are the the examples of effector and regulatory cells and what do they do?

A

Regulatory cells = regulatory t, helper t(activate other lymphocytes and phagocytes)
Effector = cytotoxic t, macrophages, other leukocytes

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39
Q

In the adaptive immune response, what destroys antigens and what retain ability to target antigens in future?

A

effector cells target: cytotoxic t

memory b and memory t helper and t cytotoxic for future

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40
Q

Finish the sentence. Class I and II MHC genes are responsible for encoding HLAs (human leukocyte antigens) which are proteins found on the cell surface that?

A

Define the patients tissue type!

makes sense for checking these with transplant patients!

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41
Q

What are the APCs that are able to express both classes of MHC molecules?

A

DCs, monocytes, macrophages, B lymphocytes

** under certain conditions endothelial cells are also able to function as APCs

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42
Q

Discuss MHC I molecules and what cells they are found on and what they present.

A

present peptide fragments to Tc cells
found on all cells (except RBCs)
**may present degraded viral protein fragments from infected cells

43
Q

Discuss MHC II molecules and what cells they are found on and what they present.

A

present peptide fragments to TH cells
found on APCs (DC, monocytes, macrophages, Bcells)
**bind fragments from pathogens that have been ENGULFED and digested during phagocytosis

44
Q

What cell functions as the primary APC?

A

macrophages

45
Q

What tissues and organs are the macrophages found?

A 
Tissue macrophages are found: 
connective tissue
lung (alveolar macrophages)
liver (Kupffer cells)
spleen
lymph nodes
peritoneum
CNS (microglial cells)
other areas
46
Q

How do macrophages initiate the adaptive immune response?

A

They are activated during innate response when they engulf and antigen, break it down and the present it on MHC II for T cell (cell mediated response) to recognize, then activate B cells and Thelper cells

47
Q

Where are DC located and how do they function?

A

Found through body in places where antigens can enter body:
langerhans cells (skin) –> transmit to nodes
follicular DCs (lymph nodes)
mucosal lining of bowel

48
Q

Where do macrophages mostly remain?

A

fixed in lymphoid organs

49
Q

What do dendritic cells do once they internalize pathogens?

A

enter lymphatics to present antigens to t cells in lymphoid organs

50
Q

What do activated T cells do to macrophages?

A

release chemicals that make macrophages secrete bactericidal chemicals and become insatiable phagocytes

51
Q

Why are DCs referred to as “professional” APCs?

A

because principal function of DCs is to present antigens and b/c DCs have the ability to induce a primary immune response in RESTING NAIVE T lymphocytes

52
Q

What APC is CRITICAL in establishment of immunological memory?
Where does it display endogenous antigens?

A

Dendritic cells

MHC I AND MHC II

53
Q

Humoral immunity is more important than cellular immunity in defending against what? Why?

A

microbes with capsules rich in polysaccharides and lipid toxins
Why?because ONLY THE B lymphocytes are capable of responding to and producing antibodies specific for many types of these molecules.

54
Q

T cells, mediators of cellular immunity, primarily respond to?

A

surface protein antigens

55
Q

What are the two things that a B cell clone turns into?

A
  1. most clone cells become plasma cells

2. memory cells

56
Q

When does the primary immune response occur? What is the time frame to mount a response? When are the peak levels for plasma Ab reached?

A
  • -occurs on 1st exposure to Ag
  • –3-6 days = lag period
  • -peak levels in 10 days then decline
57
Q

When does a secondary immune response occur? What is the time frame to mount a response? When are peak Ab levels reached? How long do Ab levels stay high?

A
  • -occurs on re-exposure to same Ag
  • -sensitized memory cells mount response in few hours
  • -peak levels reached in 2-3 days and much higher levels than primary
  • -Ab levels stay high for weeks to months
  • Ab bind with much greater affinity
58
Q

Discuss the composition of the classic structure of an antibody.

A
  • -compromised of 4 polypeptide chains with at least 2 identical antigen binding sites
  • -two identical light chains
  • -two identical heavy chains (forms the “Y”)
  • -Variable (V) regions of each arm combine to for identical antigen-binding sites
  • Constant (C) region
59
Q

What does the constant (C) region of the antibody structure determine?

A
  • the antibody class(M, A, D , G, E)
  • -cells and chemicals the Ab can bind to
  • how Ab class functions in Ag elimination
  • **Determine the EFFECTOR part of the antibody
60
Q

What is significance of V (variable) region on antibody?

A

It is where Ag-Ab binding occurs and differ from antibody to antibody

61
Q

What are properties of IgG?

A
  • -most abundant
  • -large molecule
  • -possess anti: viral, bacterial, toxin properties
  • -present in ALL body fluids
  • -readily enters tissues
  • -capable of crossing placenta(passive immunity to fetus)
62
Q

What are properties of IgA?

A
  • -primarily in secretory: sweat, saliva, tears, colostrum(milk), bronchial, gastro, prostatic, vaginal
  • -primary function is in local immunity on mucosal surfaces
  • -prevents attachment of viruses and bacteria to epithelial cells
63
Q

What are properties of IgM?

A
  • -pentamer
  • -first Ab released by plasma cells during primary response
  • -effective agglutinating agent because of numerous ag-binding sites
  • -readily fixes and activates complement
  • -first Ab to be produced by developing fetus and immature B lymphocytes
64
Q

What do high levels of IgM in the blood signify?

A

Acute infection

65
Q

What are the properties of IgD?

A
  • -monomer
  • -primarily on B cell membranes where functions as receptor
  • -function is unknown
66
Q

What are the properties of IgE?

A

–least common, binds very tightly to basophils and mast cells
–secreted by plasma cells in skin, mucosae of go and respiratory tracts, tonsils
–involved in inflammation and allergic responses by:
causing mast cell degranulation and release of chemical mediators including histamine
–essential for combating parasitic infections
–abdominal pain with increase =may want to thing worms

67
Q

What determines which foreign substances our immune system will recognize and resist?

A

GENES not antigens

68
Q

What are the forms the ab-ag complex can take on?

** are most important

A

Precipitation of ab-ag complex
**Agglutination of pathogens
**Neutralization of toxins
complement activation (classical pathway)

[leads to cell lysis and phagocytosis]

69
Q

What occurs in neutralization?

A
  • simplest mechanism
  • -ab block specific sites on viruses or bacterial endotoxins
  • -prevent ag from binding to receptors on tissue cells
  • -ab-ag complexes undergo phagocytosis
70
Q

What occurs in agglutination?

A

–ab bind same determinant on more than one cell-bound ag
–cross-linked ag-ab complexes agglutinate
ex= clumping of mismatched blood

71
Q

What occurs in precipitation?

A
  • soluble molecules are cross-linked

- -makes precipitate and subject to phagocytosis

72
Q

What is the main defense against cellular antigens???

A

Compliment fixation and activation!!!

73
Q

How does complement fixation and activation occur? What are the steps? (Think classical pathway).

A
  1. ab bind close together on cellular antigen
  2. complement binding sites trigger complement fixation on cells surface
  3. complement triggers cell lysis (MAC puts hole in cell, influx of fluid)
74
Q

What are the activated complement functions?

A
  • -amplifies inflammatory response
  • -opsonization
  • -enlists more and more defensive agents
75
Q

what are monoclonal antibodies?

A
  • -commercially prepared pure Ab
  • -produced by hybridomas
  • proliferate forever and produce single kind of ab
  • -used in research, clinical testing and **cancer treatment
76
Q

After antigen binding stimulates T cell, proliferation cannot occur until?

A

co-stimulation must occur

T-cell must bind to antigen on MHC II with CD4 or MHC i with CD8 and then also have TCR bind as well.

77
Q

What is an autograph?

A

transplant from one body site to another in the SAME PERSON (skin graft)

78
Q

What is an isograft?

A

transplant between identical twins
MHC should be identical
(ex: renal transplant)

79
Q

What is an allograft?

A

transplant between two individuals who are not identical twins (may be related like siblings or parent to child, etc.)

80
Q

What is a xenograft?

A

transplant from one species to another
(pig liver to human)
(heart transplants from baboons and chimps)

81
Q

What does the lymph fluid transport?

A

acellular fluid and cells of the immune system

82
Q

What are the two functions of the lymph system?

A
  1. Fluid handling (2-4L/24hours)

2. Immune surveillance

83
Q

What are the central (primary) lymphoid organs?

A

Bone marrow

Thymus

84
Q

What are the peripheral (secondary) lymphoid organs?

A

Lymph nodes, spleen, MALT =tonsils, Peyers patches in intestine, appendix, and respiratory, GI and reproductive systems

85
Q

What are the two ways that adaptive immunity can be acquired?

A

Active: develops by getting the vaccine (passive) or disease (active)
Passive: host receives antibodies or immune cells from another source

86
Q

What processes lymph from a discrete, adjacent anatomic site?

A

lymph nodes

87
Q

Compare and contrast lymph and serum.

A
  • Electrolytes are pretty equal (Na, K, Cl, Ca)
  • Creatinine is pretty equal
  • Glucose is pretty equal, little higher in serum
  • More cholesterol in serum
  • More Total protein in serum
  • More albumin in serum
  • Urea is higher in serum
  • IgG is higher in serum
88
Q

What are the three main determinants for filtration (lymph)?

A
  1. Net hydrostatic pressure
  2. Net oncotic pressure
  3. Capillary permeability
89
Q

What can change capillary permeability (think in terms of filtration to lymph system)?

A

Sepsis causes ARDS (adult respiratory distress syndrome)
Fever
Infection
Inflammation
Burns (destroy CT)
Toxic damage (sepsis, pancreatitis, inhalation)

90
Q

What is capillary oncotic pressure?

A

colloid osmotic pressure contributed by plasma proteins, mainly albumin

91
Q

What is interstitial oncotic pressure?

A

colloid osmotic pressure contributed by active proteins in the interstitium

92
Q

The capillary lumen has significatnly higher oncotic pressure than that of the interstitum and most blood proteins remain within capillary lumen. This means? And what is the difference and where is it favoring?

A

This leads to drawing fluid from the interstitium INTO the lumen.
Difference is about 20mmHg favoring resorption into capillary lumen.

93
Q

What can increased intravascular hydrostatic pressure cause? How?

A

Edema = from fluid overload and localized obstruction

  • -heart failure causes pulmonary edema and lower leg edema
  • -cirrhotic liver disease causes obstruction of flow from destruction of cells=portal htn=ascites
94
Q

What can decreased intravascular oncotic pressure cause? How?

A

Edema = protein loss

  • -malnutrition (intake issue or malabsorption in GI issue)
  • -liver failure (not making proteins)
  • -nephrotic syndrome (pee out proteins)
95
Q

What diseases cause lymphatic obstruction? Where will the edema occur?

A

Lymphoma
Metastatic cancers
Edema occurs DISTAL to the obstruction

96
Q

Where do neutrophils reside? What do they attack? Can they move?

A

Attack and destroy bacteria in the blood, they also go into the tissues as needed

97
Q

Where are lymphocytes stored and how long do they live?

A

Stored primarily in lymph nodes

–live weeks to months

98
Q

Where are leukocytes stored? How long do they live?

A
  • -formed in bone marrow, stored there until needed
  • granulocytes live 4-8 hours in blood, 4-5 days in tissues (life span shortened if infection)
  • -monocytes live 10-20 hours in blood, live for MONTHS in TISSUES as macrophages
99
Q

What three factors determine if phagocytosis will occur?

A
  1. Rough surface= increase phagocytosis
  2. Protective protein coat = less likely to be phagocytize
  3. Tagged with Ab or marker = increase phagocytosis
100
Q

What is in exudate?

A

combo of varying portions of necrotic tissues, dead neutrophils, dead macrophages, and tissue fluid

101
Q

What do basophils and mast cells secrete? Where are they located? What Ab has special propensity to become attached to these cells?

A

Secrete: histamine, bradykinin, serotonin
Basophils = blood
Mast cells = tissues
IgE

102
Q

What do interferons do? (IFNs)

A
  • -activated IFNs interact with specific cellular receptors, causing the expression of antivirus and immune modulatory genes.
  • -activated macrophages
    • induce B cells to switch Ig type
    • alter T-helper response
  • -inhibit cell growth
    • promote apoptosis
  • -induce an antiviral state in unaffected cells
103
Q

What cells release what interferons?

A

Alpha and beta secreted by virus infected cells

gamma is mainly secreted by T-cells, NK cells, macrophages

Allergy and Immunology (9 decks)

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