Chapter 21: Immune System Innate & Adapative Defenses Flashcards
(85 cards)
0
Q
Immune system has two intrinsic systems:
A
Innate (nonspecific)
And
Adaptive
1
Q
Immunity:
A
Resistance to disease
2
Q
Nonspecific = inflammation and sends macrophages. True or false
A
True
3
Q
Immune system:
A
Functional system rather than organ system
▪️innate and adapted price defenses intertwined
▪️release and recognize many of same molecules
▪️innate defenses do have specific pathways for certain substances
▪️innate responses release proteins that alert cells of adaptive system to foreign molecules
4
Q
Innate(non specific) has two lines of defense :
A
◼️first - external body membranes (skin and mucosae)
◼️second - anti microbial proteins, phagocytes , and other cells
▪️ inhibit spread of invaders
▪️inflammation most important mechanism
5
Q
Adaptive(specific) defense system :
A
◼️third line of defense attack PARTICULAR foreign substances
▪️takes longer to react than innate(nonspecific ) system
6
Q
Adaptive (specific) system has to immunities:
A
Humoral
And
Cellular
7
Q
Innate (non specific) had two defenses:
A
Skin barriers
And
Internal defenses
8
Q
What are two surface barriers?
A
Skin
Mucous membranes
9
Q
What are the 5 internal defenses (2nd line defense)?
A
◼️phagocytes ◼️NK cells ◼️inflammation ◼️anti microbial proteins (interferons/complement proteins) ◼️fever
10
Q
What are the humoral immunity defenses?
A
B cells
11
Q
What are the cellular immunity defenses?
A
T cells
12
Q
Inflammatory response contains which cells?
A
Macrophages
Mast cells
WBC
also inflammatory response
13
Q
Which are the most abundant phagocytes ?
A
Neutrophils most abundant but die fighting
-they become phagocytic on exposure to infectious material
14
Q
Macrophages develop from what?
A
Monocytes
15
Q
Which cells are chief phagocytic cells –robust cells?
A
Macrophage
16
Q
Mechanism of phagocytosis:
A
◼️phagocyte must adhere to particle
▪️ some microorganisms evade adherence with capsule
◼️cytoplasmic extensions bind to and engulf particle in vesicles called phagosome
◼️phagosome fuses with lysosomes = phagolysosome
17
Q
Phagocytosis steps:
A
◼️phagocyte adheres
◼️phagocyte forms pseudopods that engulf particles, forming phagosome.
◼️lysosome fuses with the phagocytic vesicles, forming phagolysosome
◼️lysosomic enzymes diver the particles leaving residual body
◼️exocytosis of the vesicles removed indigestible and residual material
18
Q
Phagocytosis pertains to which immunity?
A
Innate (non specific) neutrophils
19
Q
In phagocytosis, helper T cells cause what?
A
Release of respiratory burst, which kill pathogens resistant to lysosomal enzymes by:
▪️releasing cell killing free radicals
▪️producing oxidizing chemicals (H2O2)
▪️increasing pH and osmolarity of phagolysosome
20
Q
In phagocytosis what pierced the membrane?
A
Defending in neutrophils
21
Q
Natural Killer cells :
A
◼️Nonphagocytic
◼️attack cells that lack “self “ cell surface receptors.
▪️induce apoptosis in cancer cells and virus infected cells
◼️secrete potent chemicals that enhance inflammatory response
22
Q
The inflammatory response is triggered when?
A
Whenever body tissues are injured
23
Q
Inflammatory response disposes of what?
A
Debris and pathogens
24
Inflammatory response alerts what?
Adaptive (specific ) immune system
25
What are the 5 cardinal signs of inflammation?
```
◼️redness
◼️heat
◼️swelling
◼️pain
◼️impairment of function
```
26
Inflammatory response beings with what?
Chemicals released into ECF by injured tissues, immune cells, blood proteins
27
In inflammatory response, macrophages and epithelial cells of boundary tissues bear what?
Toll-like receptors (TLR)
28
How any types of TLR recognize classes of infecting microbes ?
11 types
29
What do activated TLRs trigger release?
Of cytokines that promote inflammation
30
What is the hallmark of non specific immunity ?
Inflammatory response
31
Inflammatory mediators:
◼️kinins, prostaglandins, and complement
▪️dilate local Arterioles (hyperemia)
-causes redness and heat if inflamed region
▪️make capillaries leaky
▪️many attract Leukocytes to area
▪️some have inflammatory roles
32
Inflammatory response : edema?
◼️ increase capillary permeability = exudate to tissues
▪️fluid containing clotting factors and antibodies
▪️causes local swelling (edema)
▪️swelling pushes on nerve endings = pain. Pain is also from bacterial toxins, prostaglandins, and kinins
▪️moves foreign material into lymphatic vessels
▪️deliver clotting proteins and complement
33
Clotting affords from fibrin mesh:
◼️scaffold for repair
| ◼️isolates injured areas so invaders cannot spread
34
Phagocytic mobilization:
◼️neutrophils lead; macrophages follow
▪️as attack continues, monocytes arrive.
-12 hrs after leaving bloodstream = macrophages
- these "late-arrivers" replace dying neutrophils and remain for cleanup prior to repair
◼️
35
What are the 4 steps to phagocyte mobilization?
1. leukocytosis: release of neutrophils from bone marrow in response to leukocytosis -inducing factors from injured cells
2. margination : neutrophils cling to walls of capillaries in inflamed area in response to CAMs
3. Diapedesis of neutrophils
4. chemotaxis : inflammatory chemicals promote positive chemotaxis of neutrophils
36
Interferons:
Family of immune modulating proteins ◼️ viral infected cells secrete IFNs to warn neighboring cells
▪️IFNs enter neighboring cells = producing proteins that block viral reproduction and degrade viral RNA
▪️IFN alpha and beta also activate NK cells
37
IFN gamma (immune interferon):
▪️secreted by lymphocytes
▪️widespread immune moralizing effects
▪️activates macrophages
38
INF indirectly fight cancer. True or false?
True , because they activate NK cells
39
What are artificial IFNs used to treat?
▪️hepatitis C
▪️genital warts
▪️multiple sclerosis
▪️hairy cell leukemia
40
Complement system :
◼️~ 20 blood proteins that circulate in inactive form
◼️include C1-C-9 , factors B, D , P , and regulatory proteins
◼️major mechanism for destroying foreign substances
◼️our cells contain complement activation inhibitors
41
Complement is what kind of shape protein?
Corkscrew produced in liver
42
Complement unleashes inflammatory chemicals that do what?
◼️Amplify all aspects of inflammatory response
◼️kills bacteria and certain other cell types by cell lysis
◼️enhances both innate and adaptive defenses
43
What are the three pathways to complement activation?
◼️classical pathway
◼️lectin pathway
◼️alternative pathway
44
Classical pathway:
◼️antibodies bind to invading organisms and to complement components
◼️called complement fixation
◼️first step in activation; more details later
45
Lectin pathway:
◼️lectins produced by innate (nonspecific ) system to recognize foreign invaders
-when bound to foreign invaders can also bind and activate complement
46
Alternative pathway :
Activated spontaneously , lack of inhibitors on microorganisms surface allows process to proceed
47
Complement activation :
◼️Each pathway involves activation of proteins in an orderly sequence
◼️each step catalyzes the next
◼️each pathway coverages on C3 , which cleaves into C3 and C3b
◼️common terminal pathway initiated that
-enhances inflammation promotes phagocytosis causing cell lysis
◼️cell lysis begins when :
▪️C3b binds to target cell➡️ insertion of complement proteins called membrane attack complex into cells membrane
▪️MAC forms and stabilizes hole in membrane ➡️ influx of water ➡️ lysis of cell
◼️C3b also causes opsonization
◼️C3b also causes other cleavage products to amplify inflammation
▪️stimulate mast cells and basophils to release histamine
▪️attract neutrophils and other inflammatory cells
48
Fever:
◼️abnormally high body temperature
◼️systemic response to invading microorganisms
◼️Leukocytes and macrophages exposed to foreign substances secrete pyrogens
◼️pyrogens act on body's thermostat in hypothalamus , raising body temperature
49
Benefits of moderate fever:
- Causes liver and spleen to sequester iron and zinc
| - increases metabolic rate ➡️ faster repair
50
Adaptive (specific ) defenses:
◼️protects against infectious agents and abnormal body cells
◼️amplifies inflammatory response
◼️activates complement
◼️must be primed by initial exposure to specific foreign substance
-priming takes time
51
Systemic:
Not restricted to initial site
52
Adaptive defenses have memory :
Stronger attack on "known" antigens
53
Humoral immunity produces what?
Produces fluid ; circulates in the body.
-blood
-bone marrow
B cells
54
Humoral immunity :
◼️antibodies produced by lymphocytes circulating freely in body fluids
◼️bind temporarily to target cell
-temporarily inactive
-mark for destruction by phagocytes or complement
◼️humoral immunity has extracellular targets
55
Antigen :
Anything that is capable of causing immune response
56
Cellular immunity (T cell):
◼️lymphocytes act against target cell
▪️directly- by killing infected cells
▪️indirectly - by releasing chemicals that enhance inflammatory response, or activating other lymphocytes or macrophages
◼️cellular immunity has cellular targets
57
Antigens:
◼️Substances that can mobilize adaptive (specific ) defenses and provoke an immune response
◼️targets of all adaptive (specific) immune responses
◼️most are large, complex molecules not normally found in body (non self)
58
Complete antigens:
◼️important functional properties:
▪️immunogenicity: ability to stimulate proliferation of specific lymphocytes
▪️reactivity : ability to react with activated lymphocytes and antibodies released by immunogenicity reactions
◼️examples: foreign protein, polysaccharides , lipids, and nucleic acids
59
Haptens(incomplete antigens):
◼️small molecules (haptens) not immunogenic by themselves (ex: peptides, nucleotides)
◼️May be immunogenic if attached to body proteins and combination is marked foreign
◼️cause immune system to mount harmful attack
◼️examples: poison ivy, animal dander , detergents , cosmetics
60
Antigenic determinants:
◼️only certain parts (antigenic determanants ) of entire antigen are immunogenic
◼️antibodies and lymphocytes receptors bind to them as enzyme binds to substrates
◼️most naturally occurring antigens have numerous antigenic determinants that
▪️mobilize several different lymphocyte populations
▪️form different kinds of antibodies against them
◼️large, chemically simple molecules ; have little or no immunogenicity
61
Where do T cells mature?
Thymus
62
Where do B cells mature?
Blood
63
Do T and B cells have to be activated?
Yes
64
MCH protein(self antigen):
Protein molecules on surface of cells not antigenic yo self but antigenic to others in transfusions or grafts
EX: MCH glycoproteins
-coded by genes of major histocompatability complex (MHC) and unique to individual
- have groove holding self - or foreign antigen (T lymphocytes can only recognize antigens that are presented on MHC proteins
65
3 types of cells in adaptive immune system:
◼️two types are lymphocytes:
▪️B lymphocytes (B cells)- humoral immunity
▪️T lymphocytes (T cells) - cellular immunity
◼️antigen-presenting cells
▪️do not respond to specific antigens
▪️play essential auxiliary role in immunity
66
5 steps to lymphocyte development , maturation, and activation ?
◼️origin-all originate in red bone marrow
◼️maturation
◼️seeding secondary lymphoid organs and circulation
◼️antigen encounter and activation
◼️proliferation and differentiation
67
Lymphocyte maturation:
◼️educated to become mature; B cells in bone marrow , T cells in thymus
▪️immunocompetence - lymphocyte can recognize one specific antigen by binding to it
- B or T cells display only own unique type of antigen receptor on surface when achieve maturity -- bind only one antigen
▪️self tolerance - lymphocytes unresponsive of own antigens
68
T cells:
◼️mature in the thymus under negative and positive selection pressure (tests)
▪️positive selection :
Selects T cells capable of recognizing self- MHC proteins (MHC restricion) destroyed by apoptosis
▪️negative selection:
Prompts apoptosis of T cells that bind to self- antigens displayed by self MHC
-ensures self-tolerance
69
B cells:
◼️B cells mature in red bone marrow
◼️positively selected if successfully make antigen receptors
◼️those that are self-reactive
-eliminated by apoptosis (colonial deletion )
70
Seeding secondary lymphoid organs and circulation:
◼️immunocompetent B and T cells not yet exposed to antigen called naive
◼️exported from primary lymphoid organs (bone marrow and thymus) to "seed" secondary lymphoid organs (lymph nodes, spleen)
- increases chance of encounter with antigen
71
Antigen encounter and activation:
◼️colonial selection:
▪️naive lymphocytes first encounter with antigen ➡️ selves for further development
▪️if correct signals present, lymphocyte will complete its differentiation
72
Proliferation and differentiation :
◼️activated lymphocyte proliferates ➡️ exact clones
◼️most clones ➡️ effector cells that fight infections
◼️few remain as memory cells
◼️B and T memory cells and effector T cells circulate continuously
73
Antigen receptor diversity:
◼️genes, not antigens, determine which foreign substance immune system will recognize.
▪️immune cell receptors result if acquired knowledge of microbes likely in environment
◼️lymphocytes make up to billion different types of antigen receptors
▪️coded for by ~25,000 genes
▪️gene segments are shuffled by somatic recombination
74
Antigen presenting cells:
◼️engulf antigens
◼️present fragments of antigens to T cells for recognition
◼️major types:
▪️dendritic cells: in connective tissue and epidermis
▪️macrophages : in connective tissue and lymphoid organs
▪️B cells
75
Dendritic cells and macrophages :
◼️dendritic cells phagocytize pathogens , enter lymphatics to present antigens to T cells in lymph node
▪️most effective antigen presenter known
▪️key link between innate and adaptive immunity
◼️macrophages widespread in lymphoid organs and connective tissues
▪️ present antigens to T cells to activate themselves into voracious phagocytes that secrete bactericidal chemicals
76
B lymphocytes do not activate what cells?
Naive T cells
77
B lymphocytes present what to T cell to assist own activation?
Antigens
78
Activation and differentiation of B cells:
◼️B activated when antigens bind to its surface receptors and cross -link them ➡️
◼️receptor -mediated endocytosis of cross linked antigen-receptor complexes (colonial selection) ➡️
◼️proliferation and differentiation into effector cells
79
Most clone cells become which cells?
Plasma cells and remaining clone cells become memory cells
80
Primary immunological memory response:
◼️cell proliferation and differentiation upon first antigen exposure
◼️lag period : 3 to 6 days
◼️peak levels of plasma antibody are reached in 10 days
◼️antibody levels then decline
81
Secondary immunological memory response:
◼️re-exposure to same region antigen gives faster, more prolonged more effective response :
▪️sensitized memory cells respond within hours
▪️antibody levels peak in two or three days at much higher levels
▪️antibodies bind with greater affinity
▪️antibody level can remain high for weeks to months
82
Active humoral (B cells) immunity:
◼️when B cells encounter antigens and produce specific antibodies against them
◼️two types if active humoral (B cell) immunity:
▪️naturally acquired- response to material or viral infection
▪️artificially acquired - response to vaccine of dead or attenuated pathogens
83
Passive humoral (B cell) immunity:
◼️ready made antibodies introduced into body
◼️B cells are not challenged by antigens
◼️immunological memory does not occur
◼️protection ends when antibodies degrade
84
Two types of passive humoral (B cell) immunity :
◼️naturally acquired - antibodies delivered to fetus via placenta or to infant through milk
◼️artificially acquired - injection or serum, such as gamma globulin. Protection immediate but ends when antibodies naturally degrade in body
