Immunology I Flashcards
(129 cards)
1
Q
Define immunity
A
resistance to disease
2
Q
What are the two intrinsic systems of the immune system?
A
innate (nonspecific) and adaptive (specific) defense system
3
Q
What is included in innate defenses?
A
skin, mucous membranes, phagocytes, fever, NK cells, antimicrobial proteins, inflammation
4
Q
What is included in the adaptive defenses?
A
humoral (b cells) and cellular (t cells) immunity
5
Q
What is the first line of defense of innate immunity?
A
skin and mucosa
6
Q
What is the second line of defense of innate immunity?
A
antimicrobial proteins, phagocytes
7
Q
What does the second line of defense of the innate immune system do?
A
inhibits spread of invaders. inflammation is most important mechanism
8
Q
What is the third line of defense?
A
adaptive system. attacks foreign substances. takes longer to react than innate
9
Q
What are some of the protective chemicals of the surface barriers?
A
skin acidity, lipids in sebum, dermcidin in sweat, HCl in stomach, lysozyme in saliva/lacrimal fluid, mucus
10
Q
What are some of the modifications of the respiratory system involved with innate defenses?
A
mucus-coated hairs in nose, cilia of upper respiratory tract sweep dust/bacteria up
11
Q
What are the internal defenses of the innate immune system?
A
phagocytes, NK cells, inflammatory response, antimicrobial proteins (interferon/complement), fever
12
Q
Describe macrophages
A
develop from monocytes to become main phagocytic cell. free macrophages wander thru tissues, fixed macrophages are permanent residents of some organs
13
Q
What is an example of a free macrophage?
A
alveolar macrophages
14
Q
What is an example of a fixed macrophage?
A
kupffer cells
15
Q
Describe neutrophils
A
become phagocytic on encountering infectious mat’l in tissues
16
Q
What is the first step of phagocytosis?
A
adherence of phagocyte to pathogen
17
Q
How is the first step of phagocytosis facilitated?
A
by opsonziation-coating of pathogen by complement or antibodies
18
Q
What is the second step of phagocytosis?
A
phagocyte forms pseudopods that engulf the particles forming phagosome
19
Q
What is the third step of phagocytosis?
A
lysosome fuses with phagocytic vesicle, forming a phagolysosome
20
Q
What is the fourth step of phagocytosis?
A
lysosomal enzymes digest the particles, leaving a residual body
21
Q
What is the fifth step of phagocytosis?
A
exocytosis of the vesicle removes indigestible and residual matl
22
Q
What are the steps for phagocyte mobilization?
A
leukocytosis, margination, diapedesis, chemotaxis
23
Q
Leukocytosis
A
release of neutrophils from bone marrow in response to leukocytosis-inducing factors from injured cells
24
Q
margination
A
neutrophils cling to the walls of capillaries in the inflamed area
25
chemotaxis
inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils
26
diapedesis
neutrophils flatten and squeeze out of capillaries
27
What are the different mechanisms that destroy pathogens by phagocytosis ?
acidification and digestion by lysosomal enzymes, respiratory burst, oxidizing chemicals
28
respiratory burst
release of cell-killing free radicals, activations of additional enzymes
29
Describe NK cells and what they do?
large granular lymphocytes. target cells that lack self receptors. induce apoptosis in cancer/virus cells. secrete potent chemicals that enhance inflammation
30
When is the inflammatory response activated?
Triggered whenever body tissues are injured or infected
31
How does the inflammatory response help the body?
prevents the spread of damaging agents, disposes of cell debris and pathogens, sets the stage for repair
32
What are the cardinal signs of acute inflammation?
redness, heat, swelling, pain (and sometimes impairment of fxn)
33
Describe the role of TLRs in inflammation?
macrophages and epithelial cells of boundary tissues have TLRs. Activated TLRs trigger the release of cytokines that promote inflammation
34
What are the different inflammatory mediators?
histamine, blood proteins, kinins, prostaglandins, leukrotrienes, and complement
35
What releases kinins, PGs, leukotrienes, and complement?
injured tissue, phagocytes, lymphocytes, basophils, and mast cells
36
How does inflammation and vasodilation relate?
inflammatory chemicals cause dilation of arterioles and increased permeability of local capillaries--->edema
37
What does exudate contain?
proteins, clotting factors, antibodies
38
What is the fxn of exudate?
moves foreign mat'l into lymph vessels, delivers clotting proteins to form a scaffold for repair and to isolate the area
39
What is the fxn of interferons and complement proteins?
attack microorganisms directly and reduce its ability to reproduce
40
Explain how interferon works with virus infected cells
viral-infected cells are activated to secrete IFNs. IFNs enter neighboring cells. Neighboring cells produce antiviral proteins that block viral reproduction
41
What are the fxns of IFNs?
anti-viral, reduce inflammation, activate macrophages and mobilize NK cells
42
What are genetically engineered IFNs used for?
antiviral agents against hepatitis and genital warts. MS treatment
43
What does complement do?
major mechanism for destroying foreign substances, amplifies inflammatory response, kills cells by lysis, enhances both nonspecific and specific defenses
44
Describe the classical pathway of complement activation
antibodies bind to invading organisms. C1 binds to the antigen-antibody complexes (complement fixation)
45
Describe the alternative pathway of complement activation
triggered when activated C3, B,D, and P interact on the surface of microorganisms
46
Where do both pathways of complement activation converge?
converge on C3 which cleaves into C3a and C3b
47
How does complement cause cell lysis?
C3b initiates formation of a membrane attack complex. MAC causes cell lysis by inducing a massive influx of water.
48
What else does C3b do besides initiate formation of MAC?
causes opsonization
49
What does C3a do?
causes inflammation
50
What are the benefits of moderate fever?
causes the liver and spleen to sequester Fe and Zn and increases BMR speeding up repair
51
Why are high fevers dangerous?
heat denatures proteins
52
How is fever initiated?
leukocytes and macrophages exposed to foreign substances secrete pyrogens. pyrogens reset the body's thermostat
53
Antigens
substances that can mobilize the adaptive defenses and provoke immune response. large, complex molecules not normally found in body
54
What are important fxnal properties of complete antigens?
immunogenicity and reactivity
55
Immunogenicity
ability to stimulate proliferation of specific lymphocytes and antibodies
56
Reactivity
ability to react with products of activated lymphocytes and antibodies released
57
What are some examples of complete antigens?
foreign protein, polysaccharides, lipids, nucleic acids
58
What are haptens (incomplete antigens)?
small molecules (peptides, nucleotides, hormones), immunogenic when attached to body proteins, cause an immune system to mount a harmful attack
59
What are some example of haptens?
poison ivy, animal dander, detergents, cosmetics
60
What are antigenic determinants and what is their fxn?
certain parts of an entire antigen that are immunogenic. antibodies and lymphocytes bind to them
61
What are self-antigens?
protein molecules on the surface of cells that are antigenic to others in transfusions or grafts. MHC proteins
62
What are MHC proteins?
coded for by genes of the major histocompatibility complex and are unique to the individual
63
Class I MHC proteins
found on virtually all body cells
64
Class II MHC proteins
found on certain cells in the immune response
65
What do MHC proteins do?
display peptides (usually self-antigens). in infected cells, they display fragments of foreign antigens
66
What do antigen presenting cells do?
do not respond to specific antigens. play essential auxiliary roles in immunity
67
Where do B cells mature?
Red bone marrow
68
Where do T cells mature?
thymus
69
What is immunocompetence?
the ability to recognize and bind to a specific antigen
70
What is self-tolerance?
unresponsiveness to self antigens
71
Describe positive selection of T cells
selects T cells capable of binding to self MHC proteins
72
Describe negative selection of T cells
prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC. ensures self-tolerance
73
What happens to self-reactive B cells?
are eliminated by apoptosis (clonal deletion), undergo receptor editing, and are inactivated if they escape bone marrow
74
How is antigen receptor diversity determined?
genes determine which foreign substances the immune system will recognize and resist
75
What is the fxn of APCs?
engulf antigens, present fragments of antigens to T cells
76
What are the major types of APCs?
dendritic cells, macrophages, B cells
77
What do activated T cells do to macrophages?
turn them into insatiable phagocytes and tell them to secrete bactericidal chemicals
78
Why are dendritic cells unique as APCs?
They are the only ones who have the ability to induce a primary immune response in naive T cells
79
What critical fxns do dentritic cells perform?
critical in the establishment of memory and maintenance of B cell fxn
80
What is the antigen challenge and where does it occur?
It's the first encounter btw an antigen and a naive immunocompetent lymphocyte. usually occurs in the spleen or lymph node
81
What is the fxn of most clone cells?
become plasma cells that secrete specific antibodies
82
What happens to clone cells that don't become plasma cells?
become memory cells. provide memory and mount immediate response to future exposures of the same antigen
83
Describe primary immune response.
occurs on the first exposure to a specific antigen. lag period of 3-6 days. peak levels of plasma antibody are reached in 10 days. antibody levels then decline
84
Describe secondary immune response
occurs on re-exposure to the same antigen. sensitized memory cells respond within hrs. Antibody levels peak in 2-3 days at higher levels. antibodies bind with greater affinity. antibody level can remain high for weeks to months
85
When does active humoral immunity occur?
when B cells encounter antigens and produce specific antibodies against them
86
Describe naturally acquired active immunity?
response to a bacterial or viral infection
87
Describe artificially acquired active immunity?
response to a vaccine of dead or attenuated pathogens
88
What is the fxn of vaccines?
provide antigenic determinants that are immunogenic and reactive.
89
Why do vaccines fail to fully establish immunological memory?
because they target only one type of helper T cell
90
Describe passive humoral immunity
B cells are not challenged by antigens, immunological memory doesn't occur
91
Describe naturally acquired passive immunity?
antibodies delivered to a fetus via the placenta or to infant thru milk
92
Describe artificially acquired passive immunity
injection of serum such as gamma globulin. protection is immediate but ends when antibodies degrade
93
What are immunoglobulins?
the gamma globulin portion of blood
94
What are antibodies?
proteins secreted by plasma cells that are capable of binding specifically with antigen detected by B cells
95
Describe the basic antibody structure
T or Y shaped. Two heavy and two light chains. Variable region is where antigen binds
96
What does the constant region of antibodies determine?
the antibody class (MADGE), the cells and chemicals that the antibody can bind to, how the antibody class fxns in antigen eliminations
97
Describe IgM
first class released during primary response. potente agglutinating agent. fixes and activates complement
98
Describe IgA
found in body secretions. helps prevent attachment of pathogens to epithelial cell surfaces
99
Describe IgD
attached to external surface of B cell. fxn as antigen receptor of B cells
100
Describe IgG
most abundant antibody. Protects against bacteria, viruses, toxins. Fixes complement. Main antibody in secondary and late primary response. Provides passive immunity to fetus
101
Describe IgE
secreted in skin, mucosa of GI and respiratory, tonsils. Binds to mast cells and basophils. When activated causes cells to release histamine that mediate inflammation and allergic rxn. fights parasites
102
What are the defense mechanisms used by antibodies?
neutralization, agglutination, precipitation, complement fixation
103
describe neutralization
antibodies block specific sites on pathogens. prevent these antigens from binding to tissue cells. antigen-antibody complexes undergo phagocytosis
104
describe agglutination
antibodies bind the same determinant on more than one cell bound antigen. cross-linked antigen-antibody complexes agglutinate
105
describe precipitation
soluble molecules are cross-linked. complexes precipitate and are subject to phagocytosis
106
What is the main antibody defense against cellular antigens?
complement fixation and activation
107
What are monoclonal antibodies?
commercially prepared pure antibody. produced by hybridomas (fusion of tumor cell and B cell)
108
What is the use of monoclonal antibodies?
proliferate indefinately and have the ability to produces a single type of antibody. used in research, clinical testing, and cancer treatment
109
What are the targets of the humoral response?
bacteria and molecules in extracellular environments
110
What are the targets of the cell-mediated response?
body cells infected by viruses/bacteria, abnormal or cancerous cells, cells of infused or transplanted foreign tissue
111
Which MHC proteins do CD4 cells bind to?
II MHC
112
Which MHC proteins do CD8 cells bind to?
class I MHC
113
How do dendritic cells obtain other cell's endogenous antigens?
engulfing dying virus-infected or tumor cells, or by importing antigens thru temporary gap jxns w/infected cells
114
Describe the role of antigen binding in T cell activation
antigen binding stimulates the T cell, but co-stimulation is required before proliferation can occur
115
What is co-stimulation?
required T cell binding to other surface receptors on an APC
116
What triggers proliferation and differentiation of activated T cell?
cytokines (IL-1/2 from APCs or T cells)
117
What happens to T cells without co-stimulation?
become tolerant to that antigen, are unable to divide, don't secrete cytokines
118
What happens to T cells that are activated?
enlarge, proliferate, and form clones. differentiate and perform fxns according to their T cell class
119
What is a crucial co-stimulatory signal for T cell activation?
B7 binding with CD28 receptor on a T cell
120
What is a B7 protein?
B7 proteins are produced on the surface of dendritic cells and macrophages when innate defenses are mobilized
121
Why is T cell apoptosis important after immune response has peaked?
activated T cells are a hazard
122
What is the fxn of cytokines?
mediate cell development, differentiation, and responses in the immune system
123
What two classes do cytokines include?
interleukins and interferons
124
Describe the fxn of IL-1
released by macrophages, co-stimulates bound T cells
125
Describe the fxn of IL-2
key growth factor, acts on cells that release it and other T cells
126
What is the role of Helper T cells?
once primed by APC antigen, they help activate T and B cells, induce T and B cell proliferation, activate macrophages and recruit other immune cells
127
What is the role of cytotoxic T cells?
directly attack and kill other cells.
128
What is the role of NK cells?
recognize lack of class I MHC, antibody coating a target cell, different surface marker on stressed cells.
129
What is the role of regulatory T cells?
dampen the immune response by direct contact or by inhibitory cytokines. important in preventing autoimmune rxns
