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Anatomy And Physiology 2 > Chapter 21: Immune System Innate & Adapative Defenses > Flashcards

Chapter 21: Immune System Innate & Adapative Defenses Flashcards

0
Q

Immune system has two intrinsic systems:

A

Innate (nonspecific)
And
Adaptive

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1
Q

Immunity:

A

Resistance to disease

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2
Q

Nonspecific = inflammation and sends macrophages. True or false

A

True

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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

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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

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5
Q

Adaptive(specific) defense system :

A

◼️third line of defense attack PARTICULAR foreign substances
▪️takes longer to react than innate(nonspecific ) system

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6
Q

Adaptive (specific) system has to immunities:

A

Humoral
And
Cellular

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7
Q

Innate (non specific) had two defenses:

A

Skin barriers
And
Internal defenses

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8
Q

What are two surface barriers?

A

Skin

Mucous membranes

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9
Q

What are the 5 internal defenses (2nd line defense)?

A 
◼️phagocytes
◼️NK cells 
◼️inflammation 
◼️anti microbial proteins (interferons/complement proteins)
◼️fever
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10
Q

What are the humoral immunity defenses?

A

B cells

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11
Q

What are the cellular immunity defenses?

A

T cells

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12
Q

Inflammatory response contains which cells?

A

Macrophages
Mast cells
WBC
also inflammatory response

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13
Q

Which are the most abundant phagocytes ?

A

Neutrophils most abundant but die fighting

-they become phagocytic on exposure to infectious material

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14
Q

Macrophages develop from what?

A

Monocytes

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15
Q

Which cells are chief phagocytic cells –robust cells?

A

Macrophage

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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

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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

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18
Q

Phagocytosis pertains to which immunity?

A

Innate (non specific) neutrophils

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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

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20
Q

In phagocytosis what pierced the membrane?

A

Defending in neutrophils

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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

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22
Q

The inflammatory response is triggered when?

A

Whenever body tissues are injured

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23
Q

Inflammatory response disposes of what?

A

Debris and pathogens

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24
Q

Inflammatory response alerts what?

A

Adaptive (specific ) immune system

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25
Q

What are the 5 cardinal signs of inflammation?

A 
◼️redness
◼️heat
◼️swelling
◼️pain 
◼️impairment of function
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26
Q

Inflammatory response beings with what?

A

Chemicals released into ECF by injured tissues, immune cells, blood proteins

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27
Q

In inflammatory response, macrophages and epithelial cells of boundary tissues bear what?

A

Toll-like receptors (TLR)

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28
Q

How any types of TLR recognize classes of infecting microbes ?

A

11 types

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29
Q

What do activated TLRs trigger release?

A

Of cytokines that promote inflammation

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30
Q

What is the hallmark of non specific immunity ?

A

Inflammatory response

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31
Q

Inflammatory mediators:

A

◼️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

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32
Q

Inflammatory response : edema?

A

◼️ 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

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33
Q

Clotting affords from fibrin mesh:

A

◼️scaffold for repair

◼️isolates injured areas so invaders cannot spread

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34
Q

Phagocytic mobilization:

A

◼️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
Q

What are the 4 steps to phagocyte mobilization?

A
  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
Q

Interferons:

A

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
Q

IFN gamma (immune interferon):

A

▪️secreted by lymphocytes
▪️widespread immune moralizing effects
▪️activates macrophages

38
Q

INF indirectly fight cancer. True or false?

A

True , because they activate NK cells

39
Q

What are artificial IFNs used to treat?

A

▪️hepatitis C
▪️genital warts
▪️multiple sclerosis
▪️hairy cell leukemia

40
Q

Complement system :

A

◼️~ 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
Q

Complement is what kind of shape protein?

A

Corkscrew produced in liver

42
Q

Complement unleashes inflammatory chemicals that do what?

A

◼️Amplify all aspects of inflammatory response
◼️kills bacteria and certain other cell types by cell lysis
◼️enhances both innate and adaptive defenses

43
Q

What are the three pathways to complement activation?

A

◼️classical pathway
◼️lectin pathway
◼️alternative pathway

44
Q

Classical pathway:

A

◼️antibodies bind to invading organisms and to complement components
◼️called complement fixation
◼️first step in activation; more details later

45
Q

Lectin pathway:

A

◼️lectins produced by innate (nonspecific ) system to recognize foreign invaders
-when bound to foreign invaders can also bind and activate complement

46
Q

Alternative pathway :

A

Activated spontaneously , lack of inhibitors on microorganisms surface allows process to proceed

47
Q

Complement activation :

A

◼️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
Q

Fever:

A

◼️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
Q

Benefits of moderate fever:

A
  • Causes liver and spleen to sequester iron and zinc

- increases metabolic rate ➡️ faster repair

50
Q

Adaptive (specific ) defenses:

A

◼️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
Q

Systemic:

A

Not restricted to initial site

52
Q

Adaptive defenses have memory :

A

Stronger attack on “known” antigens

53
Q

Humoral immunity produces what?

A

Produces fluid ; circulates in the body.
-blood
-bone marrow
B cells

54
Q

Humoral immunity :

A

◼️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
Q

Antigen :

A

Anything that is capable of causing immune response

56
Q

Cellular immunity (T cell):

A

◼️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
Q

Antigens:

A

◼️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
Q

Complete antigens:

A

◼️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
Q

Haptens(incomplete antigens):

A

◼️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
Q

Antigenic determinants:

A

◼️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
Q

Where do T cells mature?

A

Thymus

62
Q

Where do B cells mature?

A

Blood

63
Q

Do T and B cells have to be activated?

A

Yes

64
Q

MCH protein(self antigen):

A

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
Q

3 types of cells in adaptive immune system:

A

◼️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
Q

5 steps to lymphocyte development , maturation, and activation ?

A

◼️origin-all originate in red bone marrow
◼️maturation
◼️seeding secondary lymphoid organs and circulation
◼️antigen encounter and activation
◼️proliferation and differentiation

67
Q

Lymphocyte maturation:

A

◼️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
Q

T cells:

A

◼️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
Q

B cells:

A

◼️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
Q

Seeding secondary lymphoid organs and circulation:

A

◼️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
Q

Antigen encounter and activation:

A

◼️colonial selection:
▪️naive lymphocytes first encounter with antigen ➡️ selves for further development
▪️if correct signals present, lymphocyte will complete its differentiation

72
Q

Proliferation and differentiation :

A

◼️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
Q

Antigen receptor diversity:

A

◼️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
Q

Antigen presenting cells:

A

◼️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
Q

Dendritic cells and macrophages :

A

◼️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
Q

B lymphocytes do not activate what cells?

A

Naive T cells

77
Q

B lymphocytes present what to T cell to assist own activation?

A

Antigens

78
Q

Activation and differentiation of B cells:

A

◼️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
Q

Most clone cells become which cells?

A

Plasma cells and remaining clone cells become memory cells

80
Q

Primary immunological memory response:

A

◼️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
Q

Secondary immunological memory response:

A

◼️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
Q

Active humoral (B cells) immunity:

A

◼️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
Q

Passive humoral (B cell) immunity:

A

◼️ready made antibodies introduced into body
◼️B cells are not challenged by antigens
◼️immunological memory does not occur
◼️protection ends when antibodies degrade

84
Q

Two types of passive humoral (B cell) immunity :

A

◼️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

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