Immunology Flashcards

1
Q

body defence system

A

a system which combats and removes foreign cells/infectious agents (viruses, bacteria, fungi, parasites, toxins, cancerous cells)

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2
Q

what can foreign cells and infectious agents do to the host?

A

cause pathological damage and eventually kill their host if they are allowed to multiply unchecked

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3
Q

where are blood cells derived from?

A

either myeloid stem cell derived or lymphoid stem cell derived

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4
Q

3 types of blood cells

A

erythryocytes (red blood cells), platelets (megakaryocytes), and leukocytes (white blood cells)

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5
Q

types of leukocytes

A

neutrophils, eosinophils, basophils, monocytes, plasma cells & B cells, T lymphocytes, and NK cells

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6
Q

what are neutrophils, eosinophils and basophils also known as?

A

polymorphonuclear cells or granulocytes

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7
Q

where are the granulocytes and monocytes (and erythrocytes and leukocytes) derived from?

A

myeloid stem cells

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8
Q

where are plasma cells, B cells, T lymphocytes, and NK cells derived from?

A

lymphoid stem cell derived

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9
Q

what is the cellular component in immune response?

A

leukocytes (white blood cells)

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10
Q

general function of WBC

A

to provide a rapid and potent defense against any infectious agent

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11
Q

approximate number of WBC in adult human

A

7000 cells/µL

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12
Q

how can WBC count be used as a diagnostic tool to tell if there is infection present?

A

increased WBC count

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13
Q

where do WBC enter blood circulation from?

A

bone marrow or lymphoid tissue

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14
Q

how do WBC know where site of infection is?

A

chemotaxis - chemical messenger tells them where it is via attraction

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15
Q

movement of WBC from blood circulation to tissues occurs by

A

diapedesis - involves deformation of cells to pass through a small pore

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16
Q

what is the small pore in diapedesis mediated by?

A

molecules known as selectins

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17
Q

where does diapedesis occur?

A

only in the venous system (NOT ARTERIAL SYSTEM) - selectins are only present in inner part of endothelial cells of veins

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18
Q

how long do granulocytes circulate blood and exist in tissue?

A

once entered the blood, they spend 4-8 hours circulating; once in tissue, they exist for 4-5 days

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19
Q

how long do monocytes circulate blood and exist in tissue?

A

transit time of 10-20 hours in the blood; once in tissue, they enlarge (~ 5 fold) and become tissue macrophages (exist for months)

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20
Q

what happens to monocytes when they enter tissue?

A

they enlarge by 5 times and become tissue macrophages, existing in the tissue for months

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21
Q

how long do lymphocytes circulate blood and exist in tissue?

A

enter circulation continually from lymph nodes and circulate between tissues, lymphatic system, and circulation; life span of months or years

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22
Q

what are the 3 types of granulocytes?

A

neutrophils, eosinophils, and basophils

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23
Q

what do neutrophils do?

A

possess a number of antibacterial weaponry and have the ability to find bacteria/fungi and neutralize them by phagocytosis

first line of defense

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24
Q

most abundant leukocyte in blood

A

neutrophil

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25
Q

first defensive cell type to be recruited to a site of infection?

A

neutrophil

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26
Q

which granulocyte is mobilized following parasitic infection?

A

eosinophils

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27
Q

examples of parasitic infection

A

schistosomiasis and Trichinella “pork worm”

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28
Q

what do eosinophils do?

A

approach parasites and release substances that kill or weaken it such as hydrolytic enzymes; they also help detoxify inflammatory substances by releasing hydrogen peroxide

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29
Q

strongest oxidizing agent in the body (released by eosinophils)

A

hydrogen peroxide - breaks up bonds and detoxifies parasites and toxins

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30
Q

what is the circulating counterpart of tissue mast cells?

A

basophils

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31
Q

what do only mast cells produce?

A

heparin - used to prevent coagulation (anticoagulant) and facilitate removal of the fat particles

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32
Q

what do both basophils and mast cells do?

A

release histamine (and small quantities of bradykinin and serotonin) - important in allergic reaction (mediated by IgE)

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33
Q

what does bradykinin do?

A

activates the pain pathway (e.g., bee stings)

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34
Q

what does histamine do?

A

increase permeability of the cell, disrupts starling forces by increasing pore size so proteins can now move across membrane

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35
Q

where are basophils and mast cells located?

A

in circulation and in tissue, respectively

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36
Q

2 functional forms of immunity

A

1) innate immune system: first line of defense - normally sufficient to prevent disease

2) adaptive/acquired immune system: improved by repeated infection; involves specific response to the infectious agents

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37
Q

both neutrophils and macrophages are capable of

A

phagocytosis

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38
Q

examples of chemotactic factors

A

bacterial toxins, degenerative products of inflamed cells, complement complex, specific factors such as cytokines secreted by host or invading cells, foreign membrane protein triggering leukocytes

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39
Q

diapedesis is facilitated/initiated by

A

selectins and their ligands (adhesion molecules) which are present on the surface of leukocytes and endothelial cells of venous capillaries

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40
Q

when activated by chemotactic factors, what do selectins and ligands do?

A

cause leukocytes to slow down + make them sticky so they start rolling, which leads to diapedesis (searches for points to leave blood vessel to adjacent tissue)

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41
Q

what components make up the innate (natural) immune system?

A

physical barriers/factors, soluble compounds, cellular components

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42
Q

what are the physical barriers and factors in the innate immune system?

A

physical barriers: skin (most infectious agents cannot penetrate intact skin) - this is why people with burns/cuts get infections easily

physiological factors: pH, temperature, oxygen tension limit microbial growth, acids + digestive enzymes destroy ingested organisms

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43
Q

main routes of infections

A

epithelial surface of nasopharynx, gut, lungs, and genito-urinary tract

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44
Q

what are the soluble compounds involved in the innate immune system?

A

lysozyme, complement complex system, c-reactive protein, cytokines

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45
Q

lysozymes

A

enzymes that can attack bacterial cell wall (made of proteoglycan - splits the bond between N-acetylglucosamine and N-acetylmuramic acid

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46
Q

c-reactive protein

A

bind to surface of damaged cells and bacteria, promote the binding and activation of complement system

facilitate opsonization and recognition of bacteria leading to more efficient uptake by phagocytes

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47
Q

the complement complex system

A

system of ~20 serum proteins which interact in a cascade

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48
Q

what are the 3 pathways that can lead to complement activation?

A

classical pathway, alternative pathway, and the pathway involving Mannose Binding lectin on pathogen surface

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49
Q

how is the classical pathway activated?

A

by antibody-antigen complexes

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50
Q

how is the alternative pathway activated?

A

binding of complements to surface molecules of pathogens (don’t require antibodies)

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51
Q

what do all 3 pathways do to activate the complement cascade?

A

activate C3 convertase which activates the cascade

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52
Q

what are some functions of the complement complex system?

A

opsonization of bacteria, activation of mast cells and basophils, chemotaxis of white blood cells, and lysis of cells

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53
Q

cytokines

A

biochemical messengers stimulate leukocyte activity following infection - increase production of granulocytes, monocytes, and lymphocytes

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54
Q

hematopoeisis

A

blood cell production

55
Q

which 2 cytokines are pro-inflammatory, stimulate immune response, and increase hematopoeisis?

A

interleukin-1 (IL-1) and tumor necrosis factor (TNF)

56
Q

what are the cellular components which make up the innate immune system?

A

NK cells and phagocytic cells

57
Q

natural killer cells are effective against?

A

cancer cells - they are named for their ability to kill cancer cells

58
Q

natural killer cells are lymphocytes that can?

A

recognize cell surface changes (surface proteins) on virally-infected cells, foreign cells, and some tumor cells

NK cells can bind to them and kill them

59
Q

NK cells are activated by?

A

interferons (cytokines) which are produced by virally-infected cells and sometimes also by lymphocytes

60
Q

interferons are produced when?

A

very early in infection and form the first line of defense against viral infection

they act on NK cells and other cell types through specific membrane receptors influencing viral proteins and block synthesis of some proteins

61
Q

phagocyte means?

A

cells that eat - by engulfing and destroying

they have pseudopodia that deform and go around molecules/particles to ingest them via fusion + destroy them with lysozymes

62
Q

what are the phagocytic cells?

A

neutrophils and macrophages

63
Q

phagocytic activity is enhanced by?

A

opsonization

64
Q

opsonization

A

phagocytes have innate + intrinsic ability to bind nonspecifically to foreign organisms to engulf and destroy them

65
Q

recognition of foreign organisms is enhanced by

A

opsonization (i.e., depositing compounds such as complement (C3B), antibody, or both on the infectious agent - both leads to increased binding + phagocytic activity

both macrophages and neutrophils have receptors for C3B and antibody

66
Q

reticuloendothelial system

A

network formed from the phagocytic tissue macrophages and neutrophils which is found in many organs including bone marrow, spleen, and lymph nodes

67
Q

how are resident macrophages formed?

A

myeloid-derived monocytes (precursor to macrophages) enter the blood and then tissues, then become macrophages and adapt to the environment

68
Q

which locations have increased number of phagocytic cells?

A

skin and subcutaneous tissue, liver sinuses (Kupffer cells), spleen, bone marrow, lymph nodes, and alveola - increased possibility for infection

e.g., when you breathe in dust, macrophages removal these particles

69
Q

the reticuloendothelial system plays an important role in?

A

the clearance of particles and soluble substances in the circulation and tissues

these areas are concentrated with macrophages

70
Q

adaptive (acquired) immune system

A

mechanisms that provide specific immunity against individual invading agents - foreign agents contain specific chemical compounds (antigens) which provide a basis for their recognition by specific antibodies

work in concert with innate mechanisms of immunity

71
Q

antibodies are

A

gamma globulins (immunoglobulins)

72
Q

antibodies are secreted and synthesized by

A

derivatives of B cells

73
Q

antibodies are composed of

A

2 identical heavy chains and 2 identical light chains

74
Q

each antibody molecule is

A

bifunctional - fragment antigen binding + fragment crystalline

75
Q

each antibody has these 2 regions

A

fragment antigen binding (Fab) - allows specific binding to Ag

fragment crystalline (Fc) - similar in most antibodies and binds to host tissue and complements after Ab binds to Ag

76
Q

what are the 2 portions of an antibody?

A

variable portion (binds to antigen) and constant portion (binds to our own immune system)

77
Q

Fab binds to a particular part of a molecule called

A

antigenic determinant domain or epitope

78
Q

Ag-Ab reaction show what level of specificity?

A

high level but there is some level of cross-reactivity (binding not 100% but enough to activate antibody)

79
Q

what are the different classes of Ig?

A

IgG, IgA, IgM, IgD, IgE

80
Q

IgG

secondary immune response

A

major Ig (70-75% of circulating Ig), major antibody of secondary immune response and works against toxins

81
Q

IgA

major antibody in seromucous secretions

A

15-20% of circulating Ig, major Ig in sero-mucous secretion (saliva, colostrum, milk, genito-urinary secretion)

82
Q

IgM

agglutination of antigenically complex organisms

A

~10% of circulating Ig, pentameric Ig, an early antibody against antigenically complex organisms - agglutinates (clumps) for easier breakdown

83
Q

IgD

major form on B-lymphocytes

A

~1% of circulating Ig, major form on membrane of B-lymphocytes, may play a role in Ag triggering of lymphocyte differentiation

84
Q

IgE

parasitic immunity and allergic reaction

A

present on surface of basophil and mast cells, involved in parasitic immunity and allergic reaction

85
Q

adaptive immune response involves 2 types of immunity

A

humoral and cell-mediated

86
Q

humoral immunity

A

production of specific antibodies (immunoglobulins) against the invading agents by B cells

87
Q

cell-mediated immunity

A

T cells specifically destroy the invading agents (makes physical contact - like NK cells)

88
Q

where do B cells mature?

A

in bone marrow (in birds: in Bursa of fabricius)

89
Q

where do T cells develop?

A

in the thymus gland

90
Q

the adaptive immune system is based on the ability of B cells and T cells to do what?

A

B cells: to produce specific antibodies against Ag
T cells: to specifically attack Ag

91
Q

how does the body produce specific antibodies against a foreign antigen?

A

clonal selection

92
Q

there are estimated to be about _____ types of preformed B cells and T cells

A

1 million

93
Q

each B cell is capable of producing and recognizing how many types of antigens?

A

only 1 type

94
Q

B cells contain surface binding proteins that are identical to?

A

the binding domain of the antibody they produce

95
Q

in clonal selection, what happens when an antigen binds to a B cell?

A

binds and activates a preformed B-cell leading to its proliferation, producing many of the same type of B cells that secret specific antibodies against the same antigen

process is known as selection of the specific clones of antibody-producing B cells

96
Q

activation of B cells with an antigen results in?

(prior to exposure to antigen, B cells are dormant)

A

enlargement of the cells - some further differentiate and form plasma cells which proliferate and produce antibodies at an extremely rapid rate

97
Q

a number of B-lymphocytes do not form plasma cells and form what instead?

A

memory cells - have the membrane components to recognize the antigen

98
Q

together, the formation of plasma cells and memory cells after B-cell activation does what?

A

increases the population of B cells that can get activated if there is further infection by the same Ag

99
Q

secondary response

(involves immune memory)

A

subsequent exposure to the same antigen will cause a much more rapid and potent antibody response because there are more memory cells that can recognize the antigen

100
Q

the secondary response is the basis for which 2 processes?

A

acquiring immune response and vaccination (contain adjuvants - stronger immune response)

101
Q

what are the actions of antibodies?

A

agglutination, neutralization, opsonization, complement activation

102
Q

action of antibodies: agglutination/precipitation

A

multiple organisms/cells get bound together as a clump and form large insoluble complexes that are later phagocytosed

pentameric antibodies do this (IgM)

103
Q

action of antibodies: neutralization

A

antibody binds to the active molecule and alters tertiary structure or covers the active site and make it inactive (blocks viral binding sites)

104
Q

activation of complements by antibodies

A

C1-C9 a & b

binding of Ag to Ab activates complement binding sites in the Fc chain which in turn activates C1 and thereby starting a cascade of activation of various compounds (leads to lysis of pathogen)

(CLASSICAL PATHWAY)

105
Q

3 major groups of T cells

A

helper, cytotoxic (killer cells), suppressor

106
Q

helper T cells

A

secretes cytokines, including interleukins, CSF, and interferon-g

without helper T cells, the immune system would be very inefficient

107
Q

which disease develops due to helper T cell inactivation?

A

AIDS syndromes (immunodeficiency syndrome)

108
Q

cytotoxic T cells (killer cells)

A

bind to specific antigenic sites on the foreign cell surface and secrete perforin, which mediate hole formation and lead to apoptosis

109
Q

perforin

A

mediates hole formation in which cytotoxic compounds are injected - create an immunological synapse to secrete material + secondary messengers

and initiates a cascade leading to apoptosis

110
Q

what are cytotoxic T cells particularly lethal to?

A

tissue cells infected by virus - makes them important for rejection of organ transplants

111
Q

how can the immune system distinguish between foreign cells (antigen) and self?

A

membranes of all cells (except RBC) are genetically marked with characteristic proteins known as histocompatibility molecules (AKA human leukocyte antigens, HLA)

coded by a group of genes called major histocompatibility complex (MHC) - differences in MHC mark the cell as antigen

112
Q

how many MHC molecules does an individual have?

A

3-6 types out of 100+ different MHC molecules

113
Q

histocompatability

A

the chances that 2 individuals have the same combinations of MHC are small - the closer the match, the more histocompatible the tissues (only identical twins have identical MHC)

this is important for transplantation

114
Q

activation of T cells

A

antigens alone (without mediation of MHC) cannot activate T cells

antigens can only be presented by macrophages or infected cells bound to MHC receptors

115
Q

2 classes of MHC molecules

A

class-1 and class-2

116
Q

class-1 MHC

A

produced/expressed by all cells except by RBCs and recognized only by cytotoxic T cells

117
Q

class-2 MHC

A

expressed only by macrophages and B-cells and recognized only by helper T cells

118
Q

killer T cells only interact with Ag presented with which MHC and contain which coreceptor?

A

class-1 and CD8

119
Q

helper T cells only interact with Ag presented with which MHC and contain which coreceptor?

A

class-2 and CD4

120
Q

restriction of the type of T cell interacting with either class-1 and class-2 MHCs is due to?

A

presence of coreceptors (CD4 and CD8) which are proteins associated with T cell receptors for MHC

121
Q

how are B cells activated?

A

both by direct binding to antigen (clonal selection) as well as antigen presented by other leukocytes/macrophages (antigen presentation) and secretion by helper T cells

122
Q

suppressor T cells

A

act as regulatory cells - results in a reduction in the activity of helper T cells

suggested to be important for self immune tolerance

123
Q

what happens if something goes wrong with suppressor T cells?

A

leads to autoimmune disease (body starts attacking itself)

124
Q

2 possible mechanisms of immune tolerance

A

clonal deletion and clonal anergy

125
Q

clonal deletion (immune tolerance)

A

destruction of lymphocytes that have receptors for self (cells with identical MHC) during development and fetal stages

126
Q

clonal anergy (immune tolerance)

A

lymphocytes directed against self antigens may be present, but do not attack self antigen (containing identical MHC) - suppressor T cells play a role

127
Q

allergy

A

hypersensitivity - reactivity to an antigen which can result in pathologic reactions upon subsequent exposure to that particular antigen

involves mast cells/Basophils with IgE antibodies

128
Q

what causes inflammatory response in allergies?

A

histamine, bradykinin, serotonin, prostaglandins, reaction products of complement system, reaction products of blood-clotting systems and hormonal substances known as lymphokines (released by sensitized T cells)

129
Q

what do the tissue products released by mast cells/basophils that cause inflammatory response lead to?

A
  • attraction of tissue macrophages
  • increase in neutrophils (5 fold)
  • attracts monocytes from blood to enter the inflamed area and swell to become
  • macrophages (to increase phagocytic capability)
  • increase production of granulocytes and monocytes by bone marrow from committed stem cells
  • vasodilation of local blood vessels and excess blood
  • increased permeability of capabilities and increased interstitial fluid
  • clotting of interstitial fluid as a result of increase leakage of fibrinogen - “walling off”
  • swelling of tissue cells
130
Q

what does histamine do?

A

increased permeability of capillaries (even proteins can pass through membrane) which increases colloid/oncotic pressure and attracts more fluid, leading to swelling or edema

131
Q

complement is more likely to attach to the _____ (heavy; light) chains at the ends of the ______ (variable; constant) portions of the immunoglobulin molecules

A

heavy; constant

constant domain is where our own cells bind to (heavy chain in constant domain)

132
Q

where does the name C-reactive protein come from?

A

named because they bind to c-protein of pneumococci - stimulated by inflammation and infection (massive increase after infection)

133
Q

when are lysozymes released?

(lysozymes break down proteoglycan walls - break bond between N-acetylglucosamine and N-acetylmuramic acid)

NAG AND NAM

A

lysozymes are released when neutrophils/macrophages are activated