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IMMUNOLOGY AND SEROLOGY REVIEW > Part 1 > Flashcards

Part 1 Flashcards

1
Q
A

Immunology

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2
Q
  • Chinese developed a practice of inhaling powder made from smallpox scabs to induce protection.
A

1500

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3
Q
  • practice of deliberately exposing an individual to material from smallpox lesions so that a
    healthy individual when exposed to disease (small pox) the disease will be minimized
A

Variolation

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4
Q
  • Edward Jenner discovered the relationship between exposure to cowpox and immunity to smallpox (explains the phenomenon of cross-immunity)
A

17005

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5
Q

-from Latin word “vacca” which means “cow”
procedure of injecting cellular material. Edward Jenner injected individuals with material from a cowpox lesion and then exposed them from smallpox. This was based on his observation among milkmaids who were exposed to cowpox and eventually developed immunity to smallpox

A

Vaccination

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6
Q
  • development of first attenuated vaccine
A

Louis Pasteur

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7
Q
  • change of virulent to non-virulent by heat, aging or chemical means.
A

Attenuation

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8
Q

Serum Antitoxins

Cellular Immunity in TB

Phagocytosis

Immunity

Anaphylaxis

A

Emil vin Behring

Robert Koch

Ellie Metchnikoff

Paul Ehrlich

Charles Richet

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9
Q

Complement

Human Blood Group Ags

Immunologic Tolerance

Structure of Antibodies

Radioimmunosay

Major Histocompatibility Complex

Immunoregulation

Monoclonal Antibody

Antibody Diversity

Transplantation

Cytotoxic T cell -Recognition of virally infected cells
Theory of Cellular and Humoral Immunity

A

Jules Bordet

Karl Landsteiner

Macfariane Burnet ,Peter Medawar

Gerald Edelman Rodney Porter

Rosalyn Yallow

George Snell, Jean Dausset Baruj Benaceraf

Niels Jere .Georges Koehler

Cesar Milstein

Susumu Tonegawa

E.Donnall Thomas, Joseph Murray Peter Doherty ,Rolf

Zinkermagel Almoth Wright

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10
Q

is the ability of the individual to resist infection by means of normally present body functions

is a type of resistance that is characterized by specificity for each individual pathogen and the ability to remember a prior exposure, which result in an increase response upon repeated exposure

A

Natural Immunity

Acquired Immunity

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11
Q

First Line of Defense

Second Line of Defense

Third Line of Defense

A
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12
Q

Mechanical barrier retard entry of microbes
Acidic environemtn (ph 3-5) retards growth of microbes.

A

1.Skin (unbroken)

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13
Q

entraps foreign microorganisms
Cilia propel microorganisms out of the body

A
  1. Mucous membrane
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14
Q

Normal body temperature inhibits growth of some pathogens
Fever response inhibits growth of some pathogen

A
  1. Temperature
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15
Q
  1. Secretions containing Lysozymes (which cleaves bacterial cell wall)
A

о Saliva
о Tears

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16
Q

Phagocytic cells

A

Neutrophil
Monocytes
Macrophages

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17
Q

Liver:
Lung:
Spleen:
Brain and CNS:

A

Kupffer cells

Alveolar Macrophage

Splenic Macrophage

Microglial

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18
Q

Natural Antimicrobial Substances:

A
  • complement: lysis & facilitates phagocytosis
    Independent Pathway
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19
Q

Specialized Lymphocytes

A

a. T-cells
b. B-cells

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20
Q

Antibodies:

A

Immunoglobulin G
Immunoglobulin A
Immunoglobulin M
Immunoglobulin E
Immunoglobulin D

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21
Q

Natural Immune System

Cellular

Humoral

A

Mast cell
Neutrophil
Macrophages

Complement
Lysozyme
Interferon
C-Reactive protein

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22
Q

(act as an opsonin and activate the classical complement pathway)

A

C-Reactive protein

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23
Q

Adaptive Immune System

Cellular

Humoral

A

T-cell
B-cell
Plasma cell

Antibodies
Cytokines

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24
Q

early responders to foreign particles, particularly bacteria and move through vessel walls by diapedesis to site of injury; response is phagocytosis and inflammation enhanced by cvtokines

A

NEUTROPHIL

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25
Q

responder/effector cells in allergic and parasitic infections; can be involved in phagocytosis but not to large degree because the numbers of this WBC in response is low.

A

EOSINOPHIL

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26
Q

effector cells in immediate hypersensitivity reactions also can be involved in phagocytosis, but to a small degree because the number of circulating basophils is low. similar to basophils but have a longer life span, play a role in hypersensitivity reactions, binds immunoglobulin E (IgE).

A

BASOPHIL

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27
Q

Have long membranous extensions are antigen presenting cells and phagocytic, present to T cells in bloodstream or lymphoid tissue.

A

DENDRITIC CELL

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28
Q

large lobular phagocytic cells, in tissues are called macrophages.

A

MONOCYTE

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29
Q

important regulator of phagocytosis of bacteria and parasites. Secretes such as cytokines.
• Tumoricidial effects
• Antigen Presentation

A

MONOCYTE-MACROPHAGE

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30
Q

receptors recognize patterns in microbial cell walls or membranes and enance recognition by phagocytic neutrophils and monocytes

A

TOLL LIKE RECEPTORS

PATHOGEN RECOGNITION RECEPTORS

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31
Q

Lipomannans (mycobacteria)
Lipoproteins (diacy Iipopeptides; triacyl Iipopepides)
Lipoteichoic acids (Gram-positive bacteria)
Cel-wall B-glucans (bacteria and fungi)
Zymosan (fungi)

Monocytes, dendrite cels, mast cels. basophils, eosinophils

A

TLR-1:TLR-2 heterodimer

TLR-2 TLR-6 heterodimer

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32
Q

Double-stranded RNA (viruses)

NK cels

A

TLR-3

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33
Q

LPS (Gram-negatve bacteria)
LIpoteichoic acids (Gram-positive bacteria)

Macrophages, dendrite cels, mast cels, eosinophils

A

TLR4- (plus MD-2 and CD14)

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34
Q

Flagelin (bacteria)

Intestinal epithelium

A

TLR-5

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35
Q

Single-stranded FNA (vises)

Plasmacytoid dendritic cels, NK cells, eosinophis, B cells

A

TLR-7

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36
Q

Single-stranded RNA (viruses)

NK cels

A

TLR-8

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37
Q

DNA with unmethylaled CpG (bacteria and herpesviruses)

Plasmacytoid dendritic cells, eosinophis, B cells, basophils

A

TLR-9

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38
Q

Unknown

Plasmacytoid dendritic cells, easinophils, B cells, basophils

A

TLR-10

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39
Q

Prollin and profin-like proteins (Toxoplasma gondi, uropathogenic bacteria)

Macrophages, dendritic cells, Iiver, kidney, and bladder epithelial cells

A

TLR-11 (mouse only)

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40
Q
  • process of engulfment of foreign bodies
A

Phagocytosis

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41
Q
  • initiated as a result of tissue damage, either trauma or as a result of microorganism multiplication.
A

Phagocytosis

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42
Q

Phagocytosis Stages:

A
  1. Initiation and Chemotaxis
  2. Engulfment forming a Phagosome

3.Fusion of Cytoplasmic Granules and Phagosome to from Phagolysosome

  1. Digestion
  2. Excretion
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43
Q

Activated phagocyte has increased surface receptors that allow for adherence

A
  1. Initiation and Chemotaxis
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44
Q
  1. Initiation and Chemotaxis:
  2. Physical contact starts when [?] roll along until they encounter the site of injury or infection.
  3. They ADHERE to RECEPTORS on the endothelial cell wall of the blood vessel and penetrate the tissue by means of [?] which is aided by [?] (cells are attracted to the site of infection/inflammation by chemical substances such as soluble bacterial factors, complement components or C-reactive protein.
  4. When neutrophil or monocyte come into contact with the foreign particle surface it is enhanced by [?] (greek word for “ to prepare for eating”)

[?] are serum proteins that aids in the preparation of the foreign body for phagocytosis.
- coating the particle with plasma factors to speed up phagocytosis ex. CRP, complements and antibodies, C3b

A

Neutrophils

DIAPEDESIS; CHEMOTAXIS

OPSONIN

Opsonin

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45
Q

MECHANISM: opsonins neutralize the surface charge of foreign bodies making it easier cells to approach each other.

A
  1. Initiation and Chemotaxis
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46
Q

Initiation and Chemotaxis

NOTE: each phagocytic cells has a receptor for opsonins like Abs and complement.

A

a. CR3
b. Laminin receptor
c. Leucyl formyl methionyl phenylalanine receptor

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47
Q

Phagocytic cell is attracted to the invading organism by chemical mediators secreted by other immune cells .

A

Initiation and Chemotaxis

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48
Q

Process by which cells tend to move in a certain direction under the stimulation of a chemical substance “chemotaxins”

A

Initiation and Chemotaxis

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49
Q

After attachment an increase in oxygen consumption respiratory or oxidative burst occurs within the cell) as pseudopodia enclose the particle within a vacuole forming
PHAGOSOME

Phagocytic cells engulf the particle

A
  1. Engulfment forming a Phagosome
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50
Q
  1. Engulfment forming a Phagosome
    • Possible by active
A

AMOEBOID MOTION

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51
Q

Final structure is known as

A

phagosome or phagocytic vacuole

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52
Q

= foreign particle + engulfment /outflowing of the cytoplasmin

A

PHAGOSOME

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53
Q

Inhibited by large capsule activity (H. influenzae, N, meningitidis and S. pneumoniae)

Organism is enclosed in a vacuole.

A

PHAGOSOME

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54
Q
  • coating of particles with plasma factors 10 hasten phagocytosis
A

OPSONIZATION

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55
Q
  • antibodies and complement that interact with the surfaces of bacteria rendering them acceptable to the phagocyte
A

OPSONIN

56
Q

Phagosome moves toward the center of the cell

A

3.Fusion of Cytoplasmic Granules and Phagosome to from Phagolysosome

57
Q
  1. Digestion
    Released is by
A

EXOCYTOSIS

58
Q

The actual process of killing is oxygen dependent and results from the formation of bactericidal metabolites.

A
  1. Digestion
59
Q
  • minute cell particle that contain Hydrolytic enzymes and peroxidase approach the phagosome , fuse with It, rupture and discharge contents to it. Cells become degranulated as foreign materials are digested.
A
  1. Digestion
60
Q

hydrolytic enzymes found in mucus secretions and tears cleaves the Peptidoglycan layer of the bacterial cell wall.

A

LYSOSOME

61
Q

Cells become degranulated as foreign materials

A
  1. Digestion
62
Q

DIGESTION MECHANISM:
• RESTING CELLS derived energy from [?]
• IF PHAGOCYTOSIS is triggered: the respiratory burst produces energy via [?]
• The [?] change NADP to NADPH (reduced for of NADP by adding Hydrogen)
b. NADPH donates electron to oxygen in the presence of [?](a membrane-bound enzyme that is activated only when conformational change is triggered by the Microbes.
c. The [?] is formed -this is highly toxic and converted more to lethal products
d. 02 + Hydrogen ion in the presence of [?] - Hydrogen Peroxide or OH
• [?] is a bactericidal agent and more stable compared to other free radicals.
• The effect of Hydrogen Peroxide is potentiated by formation of Hypochlorite lons by action of [?] in the presence of Chloride ions

A

Anaerobic Glycolysis

oxidative metabolism.

HMP shunt

NADPH oxidase

radical 02 (superoxide)

superoxide dismutase (SOD)

Hydrogen peroxide

Myeloperoxidse

63
Q

2 MAJOR MECHANISM for the Killing of pathogen:
a. [?] or Increase Oxygen consumption by activation of Hexose Monophospahte Shunt forming oxygen radicals.
b. [?] across the membrane of Phagolysosome (NADPH oxidase depolarize the membrane allowing hydrogen and potassium lons enter the vacuole. When Hydrogen combines with Superoxides the pH increases which in tum activates proteases that kills the microbe.

A

Respiratory Burst

Alteration of charge

64
Q

is known to be central to the killing of microbes because or its dysfunction related to making an individual susceptible from recurrent and severe bacterial infections. (due to inability to phagocytose or kill ingested organism).

A

NADPH oxidase

65
Q

By products of digestion are transported to cell membrane and released outside the cell.

A
  1. Excretion
66
Q

Destruction of the Antigen
1. Formation of the Phagolysosome leading to the release of lysosomal contents including [?]
2. [?] produced by activated macrophages which is toxic to micraorganisms such as bacteria
3. Activation of the NADPH oxidase which is present in the phagosome membrane leading to the production of reactive oxygen intermediates such as [?] which are cytotoxic for microorganisms (Respiratory Burst or Increase Oxygen consumption by activation of Hexose Monophospahte Shunt forming oxygen radicals or activation of NADPH oxidase present in the phagosome membrane producing reactive oxygen intermediates like superoxide anion, hydrôgen peroxide and hydroxyl radicals which are cytotoxic to microorganisms).
4. Alteration of charge across the membrane of Phagolysosome by activating [?] (increasing the pH activating protease)

A

defensins, lactoferrin, and lysozyme

Nitric oxide

superoxide anion, hydrogen peroxide and hydroxyl radicals

NADPH oxidase

67
Q

aids healing but can also cause damage to tissue around the site of inflammation.

A

Both cellular and humoral response

68
Q

increased rate of blood flow towards site of injury

transfer of internal heat to the surface site of injury brought about by increased blood content.

due to pressure upon the sensory nerve by the exudate.

increased capillary permeability, allowing extravasation of blood fluid

due to pain interference with nerve supply and to destruction of the functioning units of the tissue.

A

RUBOR

CALOR

DOLOR

TUMOR

FUNTIO LAESA

69
Q

Stages of Inflammation

A

1, Vascular response
2. Cellular response
3.Resolution and Repair

70
Q

• first stage of inflammation

A
  1. Vascular response
71
Q

response of a Phagocytic cell / Effectors:

A
  1. Cellular response

NEUTROPHIL: ACUTE INFLAMMATION
MACROPHAGES: TISSUE MONOCYTES

72
Q

initiated by fibroblast proliferation as a result:
a. affected area may be totally repaired
b. injury may lead to the formation of an abscess with some loss of function

A
  1. Resolution and Repair
73
Q
  • opsonization, complement activation
  • removal of cholesterol
  • protease inhibitor
  • clot formation
  • binds hemoglobin
  • binds copper and oxidized iron

-opsonization, lysis

A

CRP

Serum Amyloid A

Alpha-1 antitrypsin

Fibrinogen

Haptoglobin

Ceruloplasmin

Complement C3

74
Q

SOLUBLE SUBSTANCES
Cytokines:

A

Interferon, Tumor Necrosis Factor, Interleukins, Chemokines, Transforming Growth Factor and Colony Stimulating Factor

75
Q

Regulate growth and differentiation of immune system effector cells (chemical messengers)

A

Cytokines

76
Q

Soluble proteins that regulate innate and adaptive immunity.

A

Cytokines

77
Q

Cytokines
- WITH MANY DIFFERENT EFFECTS
- OVERLAPPING EFFECTS
- COMBINED EFFECTS

A

Pleotropic
Redundant
Synergism

78
Q

Example: gp 130 - shared by IL-6, IL-11, leukemia inhibitory factor, , oncostatin M, ciliary neurotrophic factor and cardiotrophin.

A

Redundant

79
Q
  • affects the same cell that secreted it
  • affects the target cell in proximity
  • systemic effect or direct in the bloodstream
A

Autoerine effects

Paracrine effects

Endocrine effects

80
Q

Assist B-cell in commencing antibody production

A

Cytokines

81
Q

Killing tumor and target cells

A

Cytokines

82
Q

Rejecting grafts

A

Cytokines

83
Q

Stimulating hematopoiesis in bone marrow

A

Cytokines

84
Q

Initiating delayed hypersensitivity allergic reactions

A

Cytokines

85
Q

• enhance motility and promote migration of many types of white blood cells toward the source of the chemokine (chemotaxis)

A

Chemokines

86
Q

plays a key role on the initiation and development of inflammatory responses in numerous disease process.

A

Chemokines

87
Q

are known to induce chemokine production in the inflammatory response.

A

IL-6

TNF-a

88
Q

activates integrins or cell adhesion molecules, on leukocytes and leads to firm adhesion to endothelial cells.

A

Chemokines

89
Q

Chemokines: classified according to the position of N-terminal cysteine residues.

A

Alpha or CXC
Bete or CC
C chemokines or CX3C

90
Q

Has the ability to bind nearby cells and produce generalized anti-viral substances

A

Interferon

91
Q

Family of glycoproteins produced by all animals cells that exert a virus-nonspecific but host specific antiviral activity.

A

Interferon

92
Q

non-immune produced primarily in the initial innate response to viral infection

A

Type I Interferon

93
Q

Produced by virus induced leukocyte culture

A

IFN- Alpha

94
Q

IFN-Alpha Major producer:

A

NULL LYMPHOCYTE or NK CELLS

95
Q

• Produced by double stranded RNA fibroblasts

A

IFN-Beta

96
Q

IFN-Beta Major producer:

A

FIBROBLAST or ENDOTHELIAL CELL (FIBROENDOTHELIAL)

97
Q

Immune, primarily produced as a component of the specific immune response to vira and other pathogens

A

Type Il Interferon

98
Q

Produced by immunologically stimulated lymphocytes

A

IFN - Gamma

99
Q

IFN - Gamma Major Producer:

A

T CELLS

100
Q
  • cytotoxic activity against tumor cells and virally infected cells
A

Tumor Necrosis Factor

101
Q

produced by the macrophages called CATECHIN

A

TNF- Alpha

102
Q

exist in both Membrane Bound and Soluble Forms

A

TNF- Alpha

103
Q
  • mediate all cytotoxic and inflammatory effect by TNF by cell to cell contact.
A

• Membrane Bound

104
Q

causes VASODILATION AND INCREASED PERMEABILITY (RUBOR AND TUMOR)

A

TNF- Alpha

105
Q

produced by ACTIVATED MACROPHAGE AND MONOCYTES

A

TNF- Alpha

106
Q

Activate T-cells by inducing expression of MHC CLASS II MOLECULES

A

TNF- Alpha

107
Q

-enhance Ag presentation and activate T cells.

A

Vascular Adhesion Molecules and Chemokines (similar with IL-1)

108
Q

triggered by presence of LIPOPOLYSACCHARIDE FROM GRAM NEGATIVE BACTERIA

A

TNF- Alpha

109
Q

produced by CD4 + and CD8 + cells called LYMPHOTOXIN

A

TNF- Beta

110
Q

Cytokines produced mainly by T-cells for adaptive immune response.

A

Th1, Th2 and Treg (T-regulatory cells) Cytokines

111
Q

responsible for cell-mediated immunity

responsible for antibody-mediated immunity

regulates activities of Th1 & Th2 from naive T cells

A

Th1

Th2

Treg

112
Q

Clinical Assays for Cytokines

A
  1. ELISA
  2. PCR
  3. Fluorescence
  4. Microbead arrays
113
Q

Cytokines of Innate Immunity
Cytokines of Adaptive Immunity

A

IL-1
TNF-a
IL-6
Chemokines
TGF-B

Th1 cytokines
IFN-y
IL-2
Th2 cytokines
IL-4
IL-10

114
Q

Acquired / Adaptive /Specific Immunity Basic principles:

A

Diversity, Memory, Specimpity, self/non-self recognition

115
Q

Site of T and B cell maturation; CENTRAL LYMPHOID ORGAN

Site of proliferation and differentiation of T and B cells; PERIPHERAL LYMPHOID ORGAN

A

Primary Lymphoid Organ

Secondary Lymphoid Organs

116
Q

Antigen trapping sites

A

Secondary Lymphoid Organs

117
Q

CELL INVOLVED IN ADAPTIVE/ACQUIRED/SPECIFIC IMMUNITY

A

T- Lymphocytes

Natural Killer (NK) cell

118
Q

represent approximately 80% of the circulating lymphocytes in the peripheral bood

A

T- Lymphocytes

119
Q

Most circulating T cells express three of the following CD markers:

: SHEEP RBC RECEPTOR or CLASSICAL T-CELL SURFACE MARKER
: PART OF T CELL AG RECEPTOR COMPLEX
: RECEPTOR FOR MHC CLASS II MOLECULE
: RECEPTOR FOR MHC MHC MHC CLASS I MOLECULE

A

CD2

CD3

CD4

CD8

120
Q
  • early precursor from bone marrow that enter the thymds.
A

Thymocyte

121
Q

Development is by orderly rearrangement of genes coding for the antigen receptor.

A

Thymocyte

122
Q

Thymic stromal cells (involved in T-cell development: epithelial cells, macrophages, fibroblasts and dendritic cells)

A

Thymocyte

123
Q

Interaction of thymocytes with stromal cells is mediated by:

A

IL-7

124
Q

Thymocyte With early surface:

A

CD44 and CD25

125
Q

Considered a bridge between the innate and adaptive immune system because it is thought to have the same precursor as a lymphocyte but can respond to diseased cells without prior exposure to antigen.

A

Natural Killer (NK) cell

126
Q

Thought to act by recognizing a lack of MHC class I proteins on diseased or cancerous cells

A

Natural Killer (NK) cell

127
Q

Lack of these proteins along with signalers enhances the NK cell to cytolytic action against the damaged cell.

A

Natural Killer (NK) cell

128
Q

Also act by way of ADCC or recognition and lysis of antibody coated infected cells.

A

Natural Killer (NK) cell

129
Q

Important in transitional cell bridging innate and acquired response to pathogens.

A

Natural Killer Cells

130
Q

Kill and initiate CYTOLYTIC REACTION without prior exposure to antigen

A

Natural Killer Cells

131
Q

Natural Killer Cells Two subsets
- produce higher level of cytokines INF-gamma and NF alpha) and support antibody production
- higher cytotoxic activity

A

NK cell with high CD56 and low CD16

NK cell with low CD56 and high CD16

132
Q

Note: NK cells are stimulated once exposed to cytokines which Includes

A

INF-gamma, TF-alpha

133
Q

are able to distinguish a healthy cell from a infected or cancerous cell.

A

NK cells

134
Q

Delivers inhibitory signal by recognizing MHC Class I

A

Inhibitory Receptor

135
Q

Delivers signal to activate cytotoxic mechanism

A

Activating Receptor

136
Q

Triggered by lack of MHC Class I protein

Secretes PERFORIN and GRANZYMES

A

Activating Receptor

137
Q

T- cell development

B-cell Development

A
  1. Double-Negative Thymocytes
  2. Double-Positive Thymocytes
  3. Mature T-cell / Single Positive
  4. Activated T-cell
  5. Sensitized T-cell
  6. Pro-B-cell (progenitor C-cell stage)
  7. Pre-B. cell (precursor)
  8. Immature b-cell
  9. Mature B cell
  10. Activated B cell
  11. Plasma cell
  12. Memory cell

IMMUNOLOGY AND SEROLOGY REVIEW (4 decks)

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