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PATH > unit 4: immune response > Flashcards

unit 4: immune response Flashcards

1
Q

what is the immune response

A

protection against infection by recognition of SPECIFIC antigens and responding to them

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2
Q

what are PAMPs and DAMPs

A

PAMPs: pathogen-associated molecular patterns
- molecules associated with various pathogens, recognized by the innate immune system
DAMPs: damage-associated molecular patterns
- molecules associated with cellular damage or stress, act as signals to alert the immune system for repair

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3
Q

the role of skin and mucosal membranes in innate immunity

A
  • physical barriers of foreign agents
  • skin is slightly acidic to prevent the growth of some organisms
  • mucus acts as a protective coating
  • cilia help move foreign particles out of respiratory tract by “sweeping”
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4
Q

non-specific phagocytosis in innate immunity

A
  • first line of defence after epithelial barriers (skin)
  • lacks specificity and memory
  • neutrophils and macrophages are phagocytes in innate immunity
  • can be enhanced by opsonization
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5
Q

what characterizes the adaptive immune response

A
  1. specificity
  2. memory
  3. amplification
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6
Q

what are antigens

A

molecules that evoke and antibody response when introduced to a host

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7
Q

what are immunogens

A

molecules which elect an immune response
- larger, usually polysaccharides

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8
Q

what are haptens

A

smaller antigenic molecules, complex with larger carrier molecules

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9
Q

what happens when components of the body become antigenic

A

may be recognized as foreign, such as what happens in cancer
- helpful do the body can remove them
- binding of hapten allows this to happen

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10
Q

what is self tolerance

A

the lack of response to our own antigens
- clonal deletion suggests during embryonic development those lymphocytes which potentially react against self are deleted

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11
Q

what are lymphocytes

A

B cells and T cells - KEY PLAYERS in the immune response
- they proliferate when an antigen is presented to them

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12
Q

cell mediated immunity = function of T cells

A
  • T cells transform into effector T cells which destroy antigen-bearing cells
  • helper and “suppressor” T cells enhance and suppress the immune response
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13
Q

humoral immunity = function of B cells

A
  • transformation of B cells into plasma cells (antibody-producing cells)
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14
Q

what are the 4 cells of the immune response

A

lymphocytes, natural killer cells, antigen present cells, dendritic cells

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15
Q

what are the 2 types of lymphocytes

A

T cells and B cells
the T denotes “thymus dependent”
the B denotes “bursa equivalent” (bone marrow)
- thymus and bone marrow are sites of priming

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16
Q

overview of B cells

A
  • have cell surface antibody-receptor complex
  • when Ab/Ag interaction happens B cells proliferate = clonal expansion
  • clonal expansion produces plasma cells and memory cells
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17
Q

B cells: plasma cells

A
  • make antibodies specific to the antigent
  • off center nucleus and abundant basophilic cytoplasm
  • differentiate into 5 classes of immunoglobins: IgG, IgM, IgA, IgE, IgD
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18
Q

B cells: memory cells

A
  • presist for long periods of time
  • react to the antigen rapidly
  • responsible for “memory” of immunity
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19
Q

Overview of T cells

A
  • have T cell receptor complexes on the surface
  • TCR only recognizes antigens presented on another cell
  • naive T cells are activated and begin to proliferate
  • end result of activation depends on T cell activated
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20
Q

T cells: CD4+T cells - helper T cells

A
  • usually have more of these
  • secrete cytokines which influence most of the other cells in the immune system
  • these cytokines cause activation of macrophages, inflammation and proliferation
  • further divided into TH1 and TH2 cells
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21
Q

T cells: TH1 helper T cells

A
  • activated by release of IFN-gamma which activates macrophages and B cells
  • B cells then secrete antibodies to mediate phagocytosis and activate complement
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22
Q

T cells: TH2 helper T cells

A
  • activated by IL-4 which stimulates B cells to differentiate into IgE secreting plasma cells
  • IL-5 and IL-3 are also released which activates mast cells and eosinophils
  • produces a type 1 hypersensitivity reaction
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23
Q

T cells: CD8+T cells - cytotoxic T cells

A
  • directly kill virus infected cells and/or tumour cells
  • lesser role in secretion of cytokines
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24
Q

what are the roles of activated T cells

A
  1. cell mediated immunity: kill any cell who’s surface antigen they recognize
  2. “Helper” roles: cytokines they produce are “mediators” that influence functions of macrophages and lymphocytes
  3. delay hypersensitivity
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25
Q

what are natural killer cells

A
  • an innate type of lymphocyte
  • nonspecific
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26
Q

3 main features of NK cells

A
  1. Non-specific cytotoxic activity: directly kill cells without prior sensation by releasing cytotoxic granules which contain enzymes to induce apoptosis
  2. immunoregulation: interact with other immune cells by releasing cytokines to influence their function
  3. lack of antigen specific receptors: rely on a balance of activating and inhibitory signals from cells - lack of inhibitory signals = abnormal cell = NK cell activated
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27
Q

what are antigen presenting cells

A
  • include macrophages, interdigiting dendritic cells and follicular dendritic cells
  • APCs ingest the antigen and present its fragments on its surface with MHC complex
  • leads to T cell activation and lymphokine release
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28
Q

what are dendritic cells

A
  • cell in the immune response
  • follicular dendritic cells are responsible for antigen presentation and initiate the adaptive immune response
  • interdigitating dendritic cells produce cytokines which care important for the innate immune response
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29
Q

what are antibodies

A
  • molecules secreted from plasma cells after B cell differentiationto combat antigens
  • comprise of a family of serum proteins called immunoglobins
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30
Q

structure of antibodies

A
  • have a heavy and light chain
  • body is constant in all Ig classes
  • variable part = antigen-binding site (tip)
  • constant region has receptors for complement
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31
Q

how are antibodies produced around and after birth

A
  • new borns rely on passively acquired antibodies from their mother (mostly IgG)
  • IgG crosses the placenta in utero
  • at 3-4 months immunoglobins are at their lowest as maternally derived antibodies decrease (passive immunity = temporary)
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32
Q

what is colostrum

A

thick, yellow milky fluid secreted by the mammary gland
- has lots of immunoglobins which the gut of the neonate can absorb to acquire

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33
Q

how do antigens react with antibodies

A
  • once antigens enter the body the non-specific inflammatory response tries to stop the antigen
  • some antigens are carried through lymphatic flow which exposes them to macrophages and lymphocytes
  • phagocytosis happens and the antigen is presented on macrophages to T and B cells
  • T cells are activated and B cells become plasma cells to secrete antibodies
  • end result = antibody enters the blood and binds antigen
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34
Q

why might your lymph node under your jaw become enlarged in the case of a sore throat?

A
  • there is a response to an antigen stimulus
  • T and B cells are arranged into follicles, when enlarged are characteristic of a reactive node
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35
Q

what does reactive (or hyperplastic) mean

A

responding to an antigen stimulus

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36
Q

what are the effects of antigen-antibody interactions

A
  1. agglutination
  2. opsonization
  3. compliment fixation
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37
Q

antigen-antibody interactions: agglutination

A
  • formation of large clumps of Ag and Ab
  • 2 binding sites on antibodies cross-links a number of antibodies to antigens (makes phagocytosis easier)
  • if the antigen is a toxin, agglutination may neutralize the toxin
38
Q

antigen-antibody interactions: opsonization

A
  • coating of the antigen with antibody
  • allows increased phagocytosis by leukocytes with the Ab receptor
    -known as immune phagocytosis
39
Q

antigen-antibody interactions: complement fixation

A
  • a system of 9 proteins (C1-C9) form the MAC complex which punches holes in cell membranes
  • ## a cell with Ab/Ag complex initiates the complement cascade, results in cell lysis
40
Q

when would agglutination or opsonization occur rather than complement fixation

A

when antigen is cellular (e.g. bacteria) = agglutination and opsonization, cause inactivation of the antigen or its lysis
when antigen is macromolecular = complement activation, phagocytosis by scavenger cells

41
Q

what is the primary immune response

A
  • occurs after the first exposure of an antigen
  • “Lag” period between when antigen enters the body and antibody appears in the serum
  • in this lag period, B cells undergo clonal expansion so plasma cells can secrete Ab
42
Q

In the primary immune response, what is the order that antibodies are made in

A

first = IgM
second = IgG
later = all others

43
Q

what is the secondary immune response

A
  • following second exposure to the same antigen there is an accelerated response
  • No lag period, specific Ab production occurs rapidly due to memory: anamnestic response
  • IgG is the main antibody secreted here
44
Q

what is passive immunity

A

transfer of pre-formed antibody from one person to another

45
Q

what is a disadvantage of passive immunity

A

only temporary - Ab will be metabolized and removed, no memory

46
Q

3 examples of passive immunity

A
  1. Transplacental immunity: natural acquisition of Ab (IgG) across the placenta
  2. Colostral immunity: natural acquisition of Ab through milk in first few hours of life
  3. Therapeutic immunity: medical administration of Ab against an agent, toxin or byproduct - examples include snake antivenins and tetanus antitoxin
47
Q

what is active immunity

A

development of antibodies in response to an antigen
- occurs naturally with infection

48
Q

what is vaccination

A
  • altered form of the organism (e.g. inactive form) is used to induce a response
  • Reacts with the same lymphocytes that would respond to the pathogenic form if it were the “primary exposure”
  • When real exposure occurs there is a rapid increase in specific antibody level
49
Q

why are vaccinations given to babies in a series after birth

A
  • the ability to mount an active immune response is slowly developing in babies
  • Vaccinate early enough to be protective without being too early
  • if passively acquired maternal antibody levels have not declined, they block the vaccine - no immune response induced
50
Q

what is serology

A

study of antigen-antibody reactions in the lab

51
Q

what is the purpose of serological tests

A
  • look for antibodies in the patients serum, level present measured by its titer
  • titer indicates the dilution of reactivity between Ab/Ag
  • Higher Ab in serum = greater dilution of that serum = high titer
52
Q

what does the presence of serum antibodies indicate in a serological test

A

ONLY indicates previous exposure organism, not necessarily active disease

53
Q

what is a hypersensitivity reaction

A

normal protective immune responses “gone wrong”
- may be inadequately controlled, inappropriately targeted or directed at harmless antibodies
- leads to tissue damage and disordered function

54
Q

what are the 4 types of hypersensitivity reactions

A
  1. Type I: immediate hypersensitivity
  2. Type II: Antibody mediated hypersensitivity
  3. Type III: Immune-complex mediated hypersensitivity
  4. Type IV: Cell mediated hypersensitivity
55
Q

types of localized type I hypersensitivity reactions

A

Hay fever: reaction site is mucosal membranes of nasal sinuses (lead to sneezing)
Skin allergies (urticara, hives)
Allergic gastroenteritis
Asthma

56
Q

what defines Immediate (type I) hypersensitivity

A
  • often referred to as anaphylactic
  • Infiltration of eosinophils in the affected tissue - these cells release mediators responsible for the tissue injury
  • can be localized or systemic
57
Q

Systemic type I hypersensitivity reactions

A
  • more serious than localized
  • includes anaphylaxis: exposure to a small dose of antigen leads to a body-wide response
  • e.g. allergy to peanuts
58
Q

types of mediators in Type I hypersensitivity

A
  1. primary performed vasoactive mediators
  2. secondary generated lipid mediators
  3. cytokine synthesis mediators
59
Q

type I hypersensitivity: primary performed vasoactive mediators

A
  • released from mast cell granules, responsible for type I hypersensitivity
  • Most important = HISTAMINE - increases vascular permeability, vasodilation, bronchoconstriction and increased mucus secretion
60
Q

type I hypersensitivity: secondary generated lipid mediators

A
  • activated by phospholipase A - produces arachidonic acid and its metabolites from mast cell membrane phospholipids
  • also leads to platelet-activating factor production
  • causes same effects as primary mediators, except vasodilation
61
Q

type I hypersensitivity: cytokine synthesis mediators

A
  • secreted cytokines (TNF) and chemokines released from mast cells recruit and activate other inflammatory cells - amplify response
  • results in release of additional mediators, local tissue damage
62
Q

what defines antibody mediated (type II) hypersensitivity

A
  • antibody is directed against specific antigens on cell surfaces
  • when the Ab/Ag complexes cell injury can occur
  • Results from one of three different antibody dependent mechanisms… 1) Opsonization & Phagocytosis, 2) inflammation, 3) Antibody mediated Cellular Dysfunction
63
Q

examples of type II hypersensitivity diseases

A

myasthenia graves: antibodies are formed to acetylcholine receptors
graves disease: hyperthyroidism caused by antibodies binding to the TSH receptor has a stimulating effect on the release of thyroid hormone

64
Q

what is immune Hydros Fetalis

A
  • produced by Rh incompatibility
  • Complement is activated and fixation of the C56789 complex destroys cells the body needs
  • RBCs or platelets are destroyed because the antigen was attached to its surface
65
Q

what defines immune-complex mediated (type III) hypersensitivity

A
  • an antigen elicits the formation of a specific antibody, interaction between the antibody and antigen result in intravascular immune complexes
  • Immune complexes are deposited in the walls of small vessels and lead to complement activation, acute inflammation and tissue injury
  • End result = fibrinoid necrosis of small vessels
66
Q

Type III hypersensitivity: Local Immune complex diseases

A

e.g. the arthus reaction
- tissue necrosis occurs at site of antigen entry
- repeated exposure to antigen = high levels of antibody in serum
- Ab/Ag complexes are formed and deposit locally in small blood vessels
- leads to acute vasculitis and local tissue necrosis

67
Q

Type III hypersensitivity: systemic Immune complex diseases

A
  • prototype = serum sickness
  • results from exposure to large dose of antigen - when more Ag is present than Ab immune complexes are formed of a critical size
  • deposit in walls of vessels and activate complement, leading to necrosis
68
Q

what is central in pathogenesis of tissue injury

A

complement activation by Ab/Ag

69
Q

what characterizes cell mediated (type IV) hypersensitivity

A
  • mediated by SENSITIZED T cells which are either cytotoxic or helpers
    2 mechanisms - CD4+ TH1 helper T cells or CD8+ cytotoxic T cells
70
Q

Type IV hypersensitivity: helper T cell mechanism

A
  • CD4+ TH1 cells respond to tissue antigens by secreting cytokines that stimulate inflammation and activate phagocytosis
  • CD4+ TH17 cells recruit neutrophils
71
Q

Type IV hypersensitivity: cytotoxic T cells mechanism

A

CD8+ cytotoxic T cells directly kill tissue cells expressing intracellular antigens (APC)

72
Q

type IV hypersensitivity diagnostically: tuberculin test

A

Tuberculin: inactivated antigen that causes tuberculosis
- delayed reaction occurs to provide evidence of previous exposure
- Direct T cell mediated cytotoxicity is the cause of necrosis in cancer cells and other foreign cells

73
Q

what is an allograft

A

graft of tissue between 2 individuals of the same species, but different genotype

74
Q

what are histocompatibility molecules

A
  • have role in the induction and regulation of normal immune function
  • histocompatibility determines if a transplant will be successful
  • molecules bind to peptide fragments of a foreign protein for presentation to antigen-specific T-cells
  • reactivity to transplanted cells can be directed against cell surface antigens
75
Q

what are histocompatibility agents

A

HLA antigens on surfaces of nucleated cells
- coded for by MHC

76
Q

what do major histocompatibility complexes encode for

A

Class I MHC molecules: found in all tissues (e.g. HLA)
Class II MHC molecules: more restricted tissue distribution, expressed on APCs and B cells

77
Q

T cell mediated organ transplant rejection (type IV hypersensitivity)

A
  • type IV hypersensitivity reactions can lead to classic acute rejection of an organ transplant
  • Recognition of organ as foreign triggers an immune response that damages the organ
78
Q

Antibody mediated rejection of

A
  • anti-HLA antibodies are developed along with T cell mediated rejection
  • Targets vascular endothelium, platelet aggregation and coagulation - leads to ischemia
79
Q

what is an autoimmune disease

A

immune-mediated response is directed against “self” (failure of self-tolerance)

80
Q

theory for how autoimmune diseases can arise

A
  • clonal deletion phase in embryonic development being faulty
  • Individual born with clones of lymphocytes can react against normal tissue
  • failure of self tolerance can also develop if individuals have lymphocytes with receptors for self-antigens which fail to be suppressed by T suppressor cells
81
Q

what is anergy

A

inactivation of lymphocytes induced by exposure to antigens under certain conditions
- genetic and gender factors have role in predisposition to the development of AI diseases

82
Q

primary immunodeficiency disease

A
  • affects specific humoral or cellular immunity, or nonspecific innate host mechanisms
  • rare, genetically determined
  • Severe combined immunodeficiency (SCID): shows defects in humoral and cell-mediated immunity
83
Q

secondary immunodeficiency disease

A
  • can arise from malnutrition, cancers, chemotherapy, and infection
  • occur more frequently
  • most important = AIDS
84
Q

what is AIDS

A
  • acquired immunodeficiency syndrome
  • immunosuppression which leads to opportunistic infections, cancers and neurological signs
  • caused by infection with a retrovirus - HIV
85
Q

how does HIV cause AIDS

A
  • the human immunodeficiency virus transcribes its RNA into DNA and then integrates it into cellular DNA
  • DNA transcription is initiated due to exposure to antigens or cytokines
  • Anything that promotes T cell activation and growth will promote death of HIV infected cells (helper T cells)
86
Q

structure of HIV

A
  • outer lipid envelope of the HIV retrovirus is studded by gp120 and gp41
  • Inner core protein p24 is the most readily detected viral antigen of HIV
  • Antibodies used to detect it are against p24 agent
87
Q

what type of immunity does AIDS primarily affect

A

cell-mediated immunity

88
Q

what is the defining characteristic of HIV

A

Loss of CD4+ T cells

89
Q

what are some other Cell Affected HIV infections other than AIDS: infection of monocytes and macrophages

A
  • HIV can infect and multiply in non-dividing macrophages
  • Macrophages can transport HIV to other body sites, mostly nervous system
  • Dendritic cells at mucosal surfaces have important roles in viral capture and transport to lymph nodes - infect CD4+T cells
90
Q

what are major sites of infection by HIV

A

CD4+ T cells, dendritic cells, lymph nodes and macrophages

91
Q

course of HIV infection

A
  1. early acute phase: culminates in virus specific immune response, detection of virus-specific antibodies
  2. middle chronic phase: HIV test is positive but few signs of disease, viral replication continues in lymphoid tissue
  3. Final “crisis” phase: disease progresses to a severe opportunistic infection and very low CD4+ cell count, death results around 2 years after

PATH (11 decks)

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