Chapter 21 Immune System Flashcards
1
Q
Which of the following contributes to the flow of lymph through lymphatic vessels
A
The pumping of the heart
The milking action of skeletal muscle contraction*
Pressure changes in the thorax that result from breathing*
Both b and c****
All of the above
2
Q
The thymus is important for ____
A
- T lymphocyte maturation*
- removal of foreign antigens
- B lymphocyte maturation
- secretion of hormones that promote B lymphocyte immunocompetence
3
Q
Areas of the spleen that contain large aggregation of lymphocytes are known as
A
- peyers patches
- adenoids
- white pulp*
- red pulp
- lymph nodes
4
Q
Immunity
A
- bodys defense against invaders
- resistance to disease
- immune system has two intrinsic systems:
- innate
- adaptive
5
Q
innate immunity
A
- nonspecific defense system
- born with
- 1st line of defense- surface barriers- skin, mucous membranes
- 2nd line of defense- internal defenses
6
Q
adaptive immunity
A
- specific defense system
- active
- 3rd line of defense:
- humoral immunity
- cellular immunity
7
Q
Internal defenses
A
- 2nd line of innate defense
- cells and chemicals
- necessary if microorganisms invade deeper tissues
- phagocytes
- Natural Killer (NK) cells
- inflammation- inflammatory response (macrophages, mast cells, WBCs, and inflammatory chemicals)
- antimicrobial proteins (interferons and complement proteins)
- fever
8
Q
Surface barriers
A
- 1st line of innate defense
- skin (keratin)- physical barrier to most microorganisms
- mucosae provide similar mechanical barriers
- mucous membranes
- hair
- protective chemicals inhibit or destroy microorganisms
- skin acidity
- lipids in sebum and dermcidin in sweat- toxic
- stomach acids
- lysozyme of saliva and lacrimal fluid
- mucus- traps microorgansisms
9
Q
humoral and cellular immunity
A
- 3rd line of defense
- humoral immunity- B cells
- cellular immunity- T cells
10
Q
phagocytes: neutrophils and macrophages (and eosinophil)
A
- neutrophils- most common
- macrophages- develop from monocytes to become the chief phagocytic cells
- phagocyte mobilization:
- leukocytosis
- margination
- diapedesis
- chemotaxis
11
Q
phagocyte mobilization
A
- leukocytosis- neutrophils enter blood from bone marrow
- margination- neutrophils cling to capillary wall
- diapedesis- neutrophils flatten and squeeze out of capillaries
- chemotaxis- neutrophils follow chemical trail
- innate defense -> internal defense
- inflammatory chemicals diffusing from the inflamed site act as chemotactic agents
12
Q
Phagocytosis: Step 1: Adherence of phagocyte to pathogen
A
- facilitated by OPSONIZATION (to make tasty)- coating of pathogen by complement proteins or antibodies -> attracts the phagocyte
- destruction of pathogens:
- acidification and digestion by lysosomal enzymes
- respiratory burst- release of cell killing free radicals
13
Q
Natural Killer (NK) cells
A
- large granular lymphocytes
- target cells that lack self cell-surface receptors, look for ABNORMAL cells
- induce apoptosis (suicide) in cancer cells and virus- infected cells before immune system is activated
- secrete potent chemicals that enhance the inflammatory response (positive feedback)
14
Q
Inflammatory Response
A
- triggered whenever body tissues are injured or infected
- prevents the spread of damaged agents
- cardinal signs of acute inflammation:
- redness
- heat
- swelling
- pain
- (sometimes) 5. impairment of function
15
Q
Benefits of inflammation
A
- dilutes harmful substances
- brings in useful substances
- disposes of debris
- pain immobilizes
- prevent spread of damaging agents
16
Q
steps of inflammatory response
A
- tissue injury
- release of different factors and chemicals -> initiate inflammatory response (histamine, complement proteins, prostaglandins)
- vasodilation of arteries -> local hyperemia -> heat -> redness -> increased metabolic rate of cells -> increased healing
- increased capillary permeability -> leak fluid -> pain -> swelling -> possible temporary limitation of joint movement -> increased healing
- neutrophils, monocytes etc. released
- leukocytosis factors
17
Q
antimicrobial proteins
A
- interferons (IFNs) and complement proteins
- attack microorganisms directly
- hinder microorganisms ability to reproduce
18
Q
interferons
A
- interfere with viral replication
- viral infected cells are activated to secrete IFNs
- IFNs enter neighboring cells
- neighboring cells produce antiviral proteins that block viral reproduction
- activate macrophages and mobilize NK cells
- virus enters cell
- interferon genes switch on
- cells produces interferon molecules
- interferon binding stimulates cell to turn on genes for antiviral proteins
- antiviral proteins block viral reproduction
19
Q
complement activation
A
- activated complement
- enhances inflammation
- promotes phagocytosis (opsonization)
- causes cell lysis
- formation of a membrane attack complex (MAC)
- MAC causes cell lysis by inducing a massive influx of water by making a hole
- complement enhances the effectiveness of both the innate and adaptive defenses
- complement system is major mechanisms for destroying foreign substances
20
Q
fever
A
- systemic response to invading microorganisms
- leukocytes and macrophages secrete pyrogens
- pyrogens reset the body’s thermostat upward (hypothalamus)
- high fevers are dangerous because heat denatures enzymes
- benefits of moderate fever -> increases metabolic rate, which speeds up repair
21
Q
inflammation ________
A
- is caused by bacterial activity to enhance the spread of disease
- is caused by viral activity to enhance the spread of the disease
- slows the healing process with swelling that can impair bodily function
- brings more leukocytes to the sight of infection***
22
Q
interferons __________
A
- are virus-specific, so that an interferon produced against one virus could not protect cells against another virus
- act by increasing the rate of cell division
- interfere with viral replication within cells*
- are routinely used in nasal sprays for the common cold
23
Q
adaptive defenses
A
- the adaptive immune (specific defense) system - immunity to one disease doesn’t protect you against a different disease
- protects against infectious agents and abnormal body cells
- amplifies the inflammatory response
- activated complement
- specific
- systemic
- has memory
- HUMORAL
- CELLULAR
24
Q
adaptive immune system: Humoral
A
- antibody mediated
- immunity (“humors” are fluids) - B cells!
25
Q
Adaptive immune response- Cellular
A
- cell-mediated immunity
- T cells
26
Q
antigens- Antibody Generator
A
- antigens are the targets of immune response
- most are large, complex molecules not normally found in the body (nonself)
27
Q
complete antigens
A
- large molecules
- immunogenicity- can stimulate specific lymphocytes to multiply
- reactivity- ability to react with these lymphocytes and antibodies
28
Q
incomplete antigens- Haptens
A
- small molecules
- are not immunogenic
- combine with body’s own proteins and cause an attack that is harmful not protective (animal dander, detergents)
- dont react with our immune system -> combine with our own proteins
29
Q
Antigenic Determinants
A
- certain parts of an entire antigen that are immunogenic
- antibodies and lymphocyte receptors bind to them
- large, chemically simple molecules (e.g. plastics) have little or no immunogenicity
30
Q
Self-Antigens: MHC proteins
A
- protein molecules (self-antigens) on the surface of all your cells
- these are the tags that label your cells as part of your cells -> NK cells attack if lacking!
- self antigens are not foreign to you
- antigenic to others in transfusions or grafts
- MHC (major histocompatibility complex) proteins
- presence of this protein allows immune system to differentiate btw our cells and foreigners
- MHC are cells’ identity markers
31
Q
cells of the adaptive immune system: lymphocytes
A
- two types of lymphocytes: B and T lymphocytes
- B cells- humoral immunity
- T cells- cell-mediated immunity
- react to only one type of antigenic determinant
- training process is very selective -> only 2% survive
-antigen-presenting cells (APCs)
32
Q
antigen-presenting cells (APCs)
A
- do not respond to specific antigens
- play essential auxiliary roles in immunity
- dendritic cells
- macrophages
- B lymphocytes
- engulf antigens
- present fragments of antigens to be recognized by T cells -> like signal flags on their surface
33
Q
B cells
A
- form in bone marrow
- mature in RED bone marrow
- seed the secondary lymphoid organs and circulate through blood and lymph
- antigen receptors bind to antigen -> activation
- multiplies and differentiates
- memory cells or effector cells form
34
Q
T cells
A
- bone in bone marrow
- mature in thymus
- seed the secondary lymphoid organs and circulate through blood and lymph
- antigen receptors bind to antigen -> activation
- multiplies and differentiates
- memory cells or effector cells form
35
Q
Dendritic cells
A
- APCs
- capture antigens and enters lymph system to node
- most important APC
36
Q
macrophages
A
- APCs
- present antigens to t cells which activates them into voracious phagocytes
37
Q
B cells: APC
A
- APCs
- presents antigens to T cell which assists in own activation
38
Q
adaptive immunity
A
- uses lymphocytes, APCs, and specific molecules to identify and destroy Non self substances
- depends upon the ability of its cells to recognize antigens by binding to them
- communication with one another so that the whole system mounts a specific response
39
Q
Humoral immunity response
A
- antigen challenge:
- first encounter between an antigen and a naive immunocompetent lymphocyte
- usually occurs in the spleen or a lymph node
- if the lymphocyte is a B cell -> the antigen provokes a humoral immune response
- antibodies are produced
40
Q
clonal selection
A
- B cell is activated when antigen bind to its surface receptor
- stimulated B cell grows to form a clone of identical cells bearing the same antigen-specific receptors
41
Q
fate of the clones
A
- most clone cells become plasma cells
- secrete specific antibodies at the rate of 2000 molecules per second for 4-5 days
- activated B cells after meeting an antigen -> becomes a memory cell OR becomes a plasma cell (effector) cell -> becomes an antibody
42
Q
secreted antibodies
A
- circulate in blood or lymph
- bind to free antigens
- mark the antigens for destruction
- antibodies DO NOT kill antigens -> they just mark
43
Q
clones that do not become plasma cells become memory cells
A
- provide immunological memory
- mount an immediate response to future exposures of the same antigen
44
Q
immunological memory: primary immune response
A
- primary immune response
- occurs on the first exposure to a specific antigen
- lag period- 3-6 days
- peak levels of plasma antibody are reached in 10 days
- antibody levels then decline
- occurs after a delay
45
Q
immunological memory: secondary immune response
A
- occurs on re-exposure to the same antigen
- sensitized memory cells respond within hours
- antibody levels peak in 2-3 days at much higher levels
- antibodies bind with greater affinity
- antibody level can remain high for weeks to months
- more efficient, powerful, longer response
46
Q
an advantage of innate immunity is _____
A
- its barriers that prevent pathogens from entering into the body**
- the specificity of its individual cells which specialize in the removal on one type of antigen
- the numerous steps in the activation of its cells that can prevent autoimmune disease
- the use of antibodies to cause cell lysis and kill invading cells
47
Q
a sample of jons blood shows a high level of pyrogens. This would indicate that jon
A
- is feeling achy
- is producing T lymphocytes
- has a sore throat
- is running a fever*** pyrogens increase baseline temperature -> fever
- has a swollen lymph nodes
48
Q
active humoral immunity
A
- occurs when B cells encounter antigens and produce specific antibodies against them
- two types:
- naturally acquired- response to a bacterial or viral infection- direct contact
- artificially acquired- response to a vaccine of dead or attenuated pathogens
49
Q
vaccines
A
- spare us the symptoms of the primary response
- provide antigenic determinants that are immunogenic and reactive
- vaccines have wiped out smallpox and have significantly reduced measles, polio, and whooping cough
- edward jenner-
- cowpox and milkmaids
- vacca- cow
50
Q
passive humoral immunity
A
- B cells are not challenged by antigens
- antibodies “borrowed” from another source and lasts for a short period
- drawbacks:
- short lived
- does not trigger memory
- antibodies eventually are degraded
51
Q
passively naturally acquired humoral immunity
A
-antibodies delivered to a fetus via the placenta or to an infant through breast milk
52
Q
passively artificially acquired humoral immunity
A
- infection of serum, such as gamma globulin (IVIG treatments)
- protection is immediate but ends when antibodies naturally degrade in the body
- example- antivenom for treatment of poisonous snake bites
53
Q
antibodies
A
- immunoglobulins- gamma globulin portion of blood (Ig)
- proteins secreted by plasma cells (from B cells)
- capable of binding specifically with antigen detected by B cells
- all antibodies can be grouped into 1 of 5 classes:
- IgM
- IgA
- IgD
- IgG
- IgE
- MADGE
54
Q
basic antibody structure
A
- two identical heavy (H) chains (long) and two identical light chains (short)
- variable (V) regions of each arm combine to form two identical antigen binding sites
- constant (C) region determines antibody class -> (IgM, IgA, IgD, IgG, IgE)
55
Q
IgM
A
- a pentamer (large)
- first antibody released
- potent agglutinating agent in blood plasma
- readily fixes and activates complement
56
Q
IgA
A
- secretory
- monomer or dimer
- in mucus and other secretions
- found in body secretions -> saliva, sweat, milk
57
Q
IgD
A
-functions as a B cell receptor
58
Q
IgG
A
- from a secondary and late primary responses
- crosses the placental barrier
- most abundant
59
Q
IgE
A
- monomer active in some allergies and parasitic infections
- causes mast cells and basophils to release histamine
- inflammation
60
Q
Antibody targets
A
- antibodies inactivate and tag antigens (antibodies cannot destroy antigens)
- form antigen-antibody (immune) complexes
- defensive mechanisms used by antibodies
- neutralization
- agglutination
- precipitation
- lysis- complement fixation
- PLAN
61
Q
neutralization
A
- surrounds
- antibodies block specific sites on viruses or bacterial exotoxins
- prevent these antigens from binding to receptors on tissue cells
- antigen-antibody complexes undergo phagocytosis
62
Q
agglutination
A
- clumps
- cross linked antigen-antibody complexes agglutinate
- ex. clumping of mismatched blood cells
- these clumps are easily destroyed by phagocytes
63
Q
precipitation
A
- soluble small molecules are cross-linked and fall out of solution
- complexes precipitate and are subject to phagocytosis
64
Q
lysis: complement fixation and activation
A
- main antibody defense against cellular antigens
- their complement-binding sites trigger complement fixation into the cell’s surface
- complement triggers cell lysis
65
Q
which of the following best describes an antibody’s mode of action
A
- antibodies punch holes in bacterial cell membranes
- antibodies immobilize antigens and mark them for destruction*
- antibodies bind to antigens and transport them to the liver for excretion
- antibodies secrete antiviral proteins
- choice a and b are correct
66
Q
in passive immunity, the
A
- immunity system attacks normal body cells
- body is deliberately exposed to an antigen
- body receive antibodies produced by other humans*
- the body is given a dead form of the antigen
67
Q
cell-mediated immune response
A
- t cells provide defense against INTRACELLULAR antigens
- T cells:
- cause inflammation
- activate macrophages
- get other T cells fired up
- regulate much of immune system
68
Q
types of t cells
A
- helper T cells- TH
- cytotoxic T cells- TC -> destroy cells harboring foreign antigens
- regulatory T cells- TREG
- memory T cells
69
Q
comparison of humoral (B cell) and Cell-mediated response
A
- antibodies of the humoral response are the simplest ammunition of the immune response
- humoral response targets bacteria and molecules in EXTRACELLULAR environments (body secretions, tissue fluid, blood, and lymph- “humors”)
- T cells of the cell-mediated recognize and response only to processed FRAGMENTS of antigens displayed on the surface of body cells
- cell-mediated response targets body cells infected by viruses or bacteria, abnormal or cancerous cells, and cells of infused or transplanted foreign tissue
70
Q
antigen recognition
A
- immunocompetent T cells are activated when their surface receptors bind to a recognized antigen (nonself)
- t cells must simultaneously recognize:
- nonself (the antigen)
- self (an MHC protein of a body cell)
- T cells cannot see free antigens, can only recognize fragments of antigens displayed on surface of cell ( b cell can recognize in bloodstream)
71
Q
T cell activation
A
- primary T cell response peaks within a week
- T cell apoptosis occurs between days 7 and 30
- effector activity wanes as the amount of antigen declines
- benefit of apoptosis- activated T cells are a hazard
- memory T cells remain and mediate secondary responses
72
Q
activated T cells become either effector or memory T cells
A
-effector T cells -> helper, cytotoxic, regulatory
73
Q
helper T (Th) cells
A
- play a central role in the adaptive immune response
- once primed by APC presentation of antigen, they:
- help activate T cells- activated CD8 into cytotoxic T cells
- help activate B cells- B cells are useless until the helper T cell activates
- induce T and B cell proliferation
- activate macrophages and recruit other immune cells
- WITHOUT HELPER T CELLS THERE IS NO IMMUNE RESPONSE
74
Q
roles of cytotoxic T (Tc) cells
A
- only T cells that can directly attack and kill other cells
- activated cytotoxic T cells circulate in blood and lymph and lymphoid organs in search of body cells displaying antigens they recognize
- targets:
- virus infected cells
- cells with intracellular bacteria or parasites
- cancer cell
- foreign cells (transfusions or transplants)
- identifies foreign antigens on MHC 1 proteins and binds
- perforin and granzymes are released
- perforin molecules insert into target cell membrane -> forms a hole
- granzymes enter and activate enzymes that trigger apoptosis
- cytotoxic cells detach and search for another prey
75
Q
how is cytotoxic T cell mechanism of action similar to that of complement
A
- cytotoxic T cells activate B cells to produce antibodies
- cytotoxic T cells induce cell lysis with perforin a protein similar to complements MAC
- cytotoxic T cells secrete the proteins that activate complement
- cytotoxic T cells are antigen presenting cells similar to the complement proteins found of B cells
76
Q
Regulatory T (Treg) cells
A
- dampen the immune response by direct contact or by inhibitory cytokines
- important in preventing autoimmune reactions
- also called suppressor T cells
77
Q
antibodies typically act extracellular in body fluids and are therefore considered part of the humoral branch of adaptive immunity proteins
A
- true***- extracellular- humoral
- false
78
Q
disorders of immune system
A
- immunodeficiencies
- congenital and acquired conditions that cause immune cells, phagocytes, or complement to behave abnormally
- SCID, lymphoma, HIV/AIDS
- autoimmune diseases
- hypersensitivity - immediate, subacute, delayed
79
Q
SCID- severe combine immunodeficiency syndrome
A
- congenital immunodeficiency
- deficit of B and T cells
80
Q
immunodeficiencies: hodgkins disease
A
- -an acquired immunodeficiency
- cancer of the b cells
- leads to immunodeficiency by depressing lymph code cells
81
Q
acquired immune deficiency syndrome (AIDS)
A
-cripple the immune system by interfering with the activity of helper T cells
82
Q
autoimmune diseases
A
- immune system loses the ability to distinguish self from foreign
- production of autoantibodies and sensitized TC cells that destroy body tissues
- ex. multiple sclerosis, myasthenia gravis, type 1 diabetes mellitus, systemic lupus erythematous, glomerulonephritis, rheumatoid arthritis
83
Q
hypersensitivity
A
- immune responses to a perceived (otherwise harmless) threat
- causes tissue damage
- different types are distinguished by their time course and whether antibodies or T cells are involved
- antibodies cause immediate and subacute hypersensitivities
- T cells cause delayed hypersensitivity
84
Q
types of hypersensitivities
A
- immediate- local or systemic (IgE) - allergies, begins in seconds after contact
- subacute- slow onset (IgM, IgG)- mismatched blood
- delayed- onset 1-3 days- cytotoxic T cells -> ex. poison ivy
