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Immunity lectures Flashcards

1
Q

What is immunocompetence?

A

ability of body to produce robust immune response following exposure to disease-producing agents

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2
Q

What are the main functions of innate immunity?

A
  • rapid, non-specific defense against pathogens
  • eliminate damaged or necrotic cells
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3
Q

What are physical barriers of innate immunity?

A
  • skin
  • mucus membranes
  • nasal hairs
  • respiratory tract cilia
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4
Q

What are chemical barriers of innate immunity?

A
  • skin pH
  • mucus secretions
  • gastric acids
  • tears
  • sweat
  • saliva
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5
Q

What are effector cells of innate immune response?

A
  • neutrophils
  • macrophages
  • NK cells
    (complement proteins)
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6
Q

How does the innate immune system recognize pathogens?

A

PAMPS & DAMPS
- patterns unique to survival, virulence, or ability to invade // damaged or necrotic

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7
Q

What is the function of neutrophils in innate immune response?

A
  • first cell to respond (bacterial & fungal)
  • short-lived
  • phagocytose: dead cells, debris, tumor cells, pathogens, foreign materials
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8
Q

What is the function of dendritic cells in the innate immune response?

A
  • present antigens to T cells (cytoplasmic processes)
  • abundant in epithelium & mucus membranes
  • help shape adaptive immune response
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9
Q

What is the function of macrophages in the innate immune response?

A
  • phagocytose: dead cells, debris, tumor cells, pathogens, foreign material
  • release cytokines to activate other immune cells
  • may present antigens to T cells
  • long-lived in extravascular tissue
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10
Q

What is the function of NK cell in the innate immune response?

A
  • rapidly attacking & killing infected cells
  • induce apoptosis
  • release cytokines to activate immune cells
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11
Q

What is the main difference between cytotoxic T cells & NK cells?

A

NK cells do not require MHC or antibodies to kill

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12
Q

What the 3 complement pathways?

A

classical, lectin, alternate

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13
Q

Which complement pathway is a component of the adaptive immune system? Why?

A

classical because activated by antibodies bound to microbes/antigens

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14
Q

Describe the alternate pathway of complement system?

A

activated when complement proteins activated on microbe surfaces (innate)

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15
Q

Describe the lectin pathway of complement system?

A

activated when mannose binding lectin binds surface glycoproteins on microbes (innate)

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16
Q

What are the functions of the complement system?

A
  • opsonization (C3b) & phagocytosis
  • inflammation (C3a & C5a) chemoattractant for leukocytes
  • cell lysis via MAC
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17
Q

What are the functions of cytokines in innate immunity?

A
  • mediate immune & inflammatory reactions
  • communicate b/w cells
  • secreted in small amounts
  • autocrine & paracrine actions
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18
Q

What is the source & target of the cytokine TNF?

A

source: macrophage, T cells, mast cells
target: endothelial cells & neutrophils (inflammation)

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19
Q

What is the source & target of the cytokine IL-1?

A

source: macrophages & dendritic cells
target: endothelial cells (inflammation)

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20
Q

What is the source & target of the cytokine IL-12?

A

source: dendritic cells & macrophages
target: NK & T cells (increase cytotoxic activity/ increase IFN-y secretion)

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21
Q

What is the source & target of the cytokine IFN-y?

A

source: NK cells
target: activate macrophages

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22
Q

What type of innate immune reaction is elicited by extracellular bacteria or fungi?

A

inflammatory & complement

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23
Q

What type of innate immune reaction is elicited by intracellular bacteria?

A

phagocytosis

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24
Q

What type of innate immune reaction is elicited by viruses?

A

Type I interferon & NK cells

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25
Q

What are membrane bound innate immune system receptors? What do they recognize?

A

TLR –> LPS
C type lectin –> fungal polysaccharides

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26
Q

What are endosomal receptors of innate immune system? What do they recognize?

A

TLR: viral RNA/DNA

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27
Q

What are cytosolic receptors of innate immune system? What do they recognize?

A

NOD-like: necrotic cell products, ion disturbances, microbial products

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28
Q

What are primary lymphoid organs?

A

bone marrow & thymus

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29
Q

What are secondary lymphoid organs & what occurs here?

A

lymph nodes, Peyer’s patch, spleen, Waldeyer’s ring
– where adaptive immunity is initiated (lymphocytes contact antigens)

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30
Q

What constitutes Waldeyer’s Ring?

A

lingual tonsils, palatine tonsils, pharyngeal tonsils

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31
Q

Where are the majority of lymphocytes located in a healthy individual?

A

lymph nodes

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32
Q

What are the difference between innate & adaptive immunity?

A

innate = first line / nonspecific
- develops quickly
- responds rapidly
- NO memory
adaptive = specialized
- develops slower
- mediates effective defense
- memory for future encounters

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33
Q

Cells of adaptive immunity?

A
  • B lymphocytes, plasma cells, antibodies
  • Dendritic cells, T lymphocytes
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34
Q

What does the adaptive immune system recognize?

A
  • antigens
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35
Q

What types of receptors are in the adaptive immune system?

A

TCR

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36
Q

T/F the innate & adaptive immune systems can discriminate self from non-self?

A

true

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37
Q

Where do lymphocytes recognize microbes/antigens?

A

lymphoid organs

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38
Q

What is the location/distribution of T cells & B cells within a lymph node?

A

B cells: follicular region (outside)
T cells: parafollicular region (just inside B cell region)

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39
Q

Where are antibodies secreted?

A

circulation & mucosal surfaces

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40
Q

What are the functions of antibodies?

A
  • neutralize & eliminate microbes & toxins
  • prevent infection from being established
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41
Q

How do B cells recognize antigens?

A

through membrane bound IgM

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42
Q

What types of chemical structures can B cells recognize?

A
  • soluble or cell-associated proteins, lipids, polysaccharides, nucleic acids, small chemicals
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43
Q

Characteristics of IgG antibodies?

A
  • most abundant
  • opsonizer
  • crosses placenta
  • found in blood & serum
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44
Q

Characteristics of IgA antibodies?

A
  • found in mucus membrane secretions
  • forms dimer when secreted
  • neutralizing (prevents pathogen from entering cell)
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45
Q

Characteristics of IgM antibodies?

A
  • largest
  • first produced in response to antigen
  • most efficient to activate complement
  • secreted as pentamer
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46
Q

Characteristics of IgE antibodies?

A
  • function against helminths
  • mediate allergic rxn (Type I)
  • least common
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47
Q

When does rearrangement & assembly of gene segments in antibodies occur?

A

in Pre-B cell stages during development

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48
Q

When does antibody class switching occur?

A

after stimulated by antigen & CD4 T cell

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49
Q

Describe antibody class switching.

A
  • maintains antigen specificity (variable)
  • alters heavy chain to broaden functional capabilities
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50
Q

Describe the stages from B cell encountering antigen to secretion of antibodies.

A
  • B cell triggered when encounters matching antigen
  • engulfs antigen, digests it, presents fragments bound to MHC
  • antigen-MHC attracts matching T cell
  • T cell secretes cytokines helping B cell to multiply & mature into plasma cell
  • antibodies secreted into blood searching for matching antigens
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51
Q

T/F memory B cells secrete antibodies?

A

false…rapidly differentiate into Ab secreting cells upon re-exposure

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52
Q

What is the goal of vaccination?

A

stimulate adaptive immune response against microbes

53
Q

What are the main types of vaccines?

A

live-attenuated, killed/inactivated, mRNA
component / whole

54
Q

What type of vaccine is not good for immunocompromised populations?

A

live-attenuated: because only weakened virus

55
Q

What are the differences between active & passive immunity?

A

active: antibodies produced by response to antigen / long-term immunity with memory cells
- natural: infected
- artificial: vaccine

passive: antibodies derived from another source / short term with NO memory cells produced
- maternal Ab from mom to fetus

56
Q

What types of microbes does the cell-mediated response combat?

A

intracellular: microbes ingested by phagocytes
– some bacteria resist microbicidal activity // viruses replicating in cytoplasm

57
Q

Describe the sequence of events in cell-mediated immunity.

A
  • APC travel to lymphoid tissue
  • present antigen via MHC
  • T cell activated, proliferate, differentiate into effector & memory
  • T cells migrate to site of infection (CD4 & 8)
  • some remain in lymphoid tissue to help B cells produce antibodies or become memory T cells
58
Q

What is the MHC?

A
  • displays peptide antigens for recognition by T lymphocytes
  • helps recognize between self & non-self
  • locus of polymorphic genes on chromosome 6
59
Q

Where are class I / II MHC molecules found and which cells recognize them?

A

Class I: all nucleated cells –> CD8 T cells
Class II: on APC surface –> CD4 T cell
– macrophage, dendritic cell, B cell

60
Q

T/F cells with class II MHC also have class I MHC?

A

true

61
Q

What are the defining cytokines for Th1 cells?

A

IFNy

62
Q

What are the defining cytokines for Th2 cells?

A

IL-4,5 & 13

63
Q

What are the defining cytokines for Th17 cells?

A

IL-17, 22

64
Q

What are the target cells for Th1, Th2, & Th17 cells?

A

Th1: macrophage
Th2: eosinophils
Th17: neutrophils

65
Q

What type of pathogens do Th1, Th2, & Th17 cells defend against?

A

Th1: intracellular pathogens
Th2: helminths/parasites
Th17: extracellular pathogens

66
Q

As you get older how does the % of naive T cells & memory T cells change?

A

naive decreases
memory increases

67
Q

Describe how the immune response declines.

A
  • response is self-limited
  • effector lymphocytes die by apoptosis after microbe is eliminated
  • allows return to resting state
68
Q

What term describes a lack of response to antigens that is induced by exposure of lymphocytes to these antigens?

A

immunologic tolerance

69
Q

What happens if the ability to discriminate between self & non-self fails / failure of immune tolerance?

A

autoimmunity

70
Q

Under normal conditions microbes are ______ & self-antigens are _______.

A

immunogenic // tolerogenic

71
Q

Describe what occurs in central tolerance of T cells.

A
  • occurs within bone marrow / thymus
  • recognize self-antigen with high affinity –> eliminate
  • recognize self-antigen with moderate affinity –> regulatory T cell & enter peripheral tissue
72
Q

How do regulatory T cells act in peripheral T cell tolerance?

A
  • block activation of self-reactive lymphocytes
    – deplete cytokines for activation of immune cells
    – express receptors that lower affinity for immune cells to respond to self-antigens
73
Q

How does anergy work in peripheral T cell tolerance?

A

inactivation of T cells (lack of co-stimulation)

74
Q

How does deletion work in peripheral T cell tolerance?

A

apoptosis of self-reactive lymphocytes

75
Q

What are the mechanisms of peripheral T cell tolerance?

A

T regulatory cells
anergy
deletion

76
Q

What are the mechanisms of central B cell tolerance?

A
  • receptor editing (light chain)
  • negative selection (apoptosis)
77
Q

What are the mechanisms of peripheral B cell tolerance?

A
  • anergy
  • exclusion from lymphoid follicles
78
Q

What role do T cells play in B cell tolerance?

A

T cells recognize proteins on MHC of APC & activate B cells to produce antibodies
T cells also help provide stimuli for survival

79
Q

Development of autoimmunity may be related to what?

A
  • inheriting susceptibility genes –> failed self-tolerance
  • environmental triggers
    **multifactorial
80
Q

Most autoimmune diseases are associated with what genetic factors?

A
  • polygenic
  • HLA genes –> inefficient at displaying self-antigen
    – defective T cell negative selection
    – failure to stimulate regulatory T cells
81
Q

How might infections activate self-reactive lymphocytes?

A
  • increased production of co-stimulatory molecules on APCs
  • molecular mimicry
82
Q

What is a hypersensitivity reaction?

A
  • inadequately controlled immune response –> injurious/pathologic
  • directed against harmless antigen (foreign or self)
83
Q

What is a Type I hypersensitivity reaction?

A
  • tissue rxn occurs rapidly after interaction of antigen with IgE antibody bound to mast cell
  • often develop in atopic individuals (sensitized to allergen)
  • mild to severe
84
Q

What are the steps that lead to a type I hypersensitivity reaction?

A
  • allergen introduced & recognized by APC
  • APC presents to B cell / naive T cell –> Th2 cell
  • B cell class switches to IgE secreting plasma cell
  • IgE binds FcR on mast cell (primed)
  • REPEAT exposure
  • allergen binds directly to IgE primed mast cell
  • mast cell activated & releases mediators
  • immediate & late phase responses occur
85
Q

What are the chemical mediators of Type I hypersensitivity reactions?

A

vasoactive amines, lipid mediators (immediate)
cytokines (late: 2-24 hrs)

86
Q

Type I hypersensitivity vasoactive amines?

A
  • histamine!! –> vascular permeability, vasodilation, smooth muscle contraction, mucus secretions
87
Q

Type I hypersensitivity lipid mediators?

A

prostaglandins & leukotrines: smooth muscle contraction & vascular permeability

88
Q

Type I hypersensitivity cytokines?

A

TNF, chemokines, IL-4 & 5 (amplify Th2 rxn)

89
Q

What are some clinical syndromes that can occur due to Type I hypersensitivity rxns?

A
  • anaphylaxis –> fall in BP (dilation), airway obstruction (laryngeal edema)
  • bronchial asthma –> airway obstruction (hyper-smooth muscle), inflammation/tissue injury (late phase)
  • allergic rhinitis, sinusitis (hay fever) –> mucus secretions / inflammation
  • food allergies –> increased peristalsis, vomiting, diarrhea
90
Q

How do people develop allergies?

A
  • susceptibility is genetically determined
  • atopic individuals: higher serum IgE & Th2 cells
  • 50% family history of allergy
  • environment can sensitize cells
91
Q

What are type II sensitivity reactions caused by?

A

antibodies directed against target antigens on cell surfaces
- target cells for phagocytosis (opsonization)
- activate complement system (recruit neutrophils/macrophages) inflammation/tissue injury
- interfere with normal cellular functions

92
Q

Describe how type II sensitivity reactions can interfere with cellular functions?

A
  • antibody inhibits binding of NT (Ach) to receptor
  • antibody stimulates receptor without hormone
93
Q

Which diseases are examples of Antibody-Mediated Type II hypersensitivity

A
  • autoimmune hemolytic anemia
  • autoimmune thrombocytopenic purpura
  • pemphigus vulgaris
  • vasculitis by ANCA
  • Goodpasture syndrome
  • acute rheumatic fever
  • myasthenia gravis
  • graves disease (hyperthyroidism)
  • pernicious anemia
94
Q

Describe pemphigus vulgaris disease

A
  • proteins in intercellular junctions of epidermal cells (desmoglein) targeted
  • skin vesicles (bullae)
95
Q

Describe myasthenia gravis

A
  • inhibits binding of acetylcholine to receptors
  • muscle weakness & paralysis
96
Q

Describe Graves disease.

A
  • stimulates TSH receptor
  • hyperthyroidism
97
Q

What are type III hypersensitivity reactions?

A
  • immune complex (antigen-antibody)
  • deposits in blood vessels –> complement activation & inflammation
  • foreign or endogenous
  • soluble antigens (in blood)
98
Q

What are examples of immune complex mediated diseases?

A
  • systemic lupus erythematous
  • arthus reaction
  • poststreptococcal glomerulonephritis
  • polyarteritis nodosa
  • reactive arthritis
  • serum sickness
99
Q

Describe arthus reaction.

A
  • various foreign proteins act as antigen –> typically from vaccine
  • manifests as cutaneous vasculitis
100
Q

What cells are involved in type IV hypersensitivity reactions?

A

T cells
- CD4: cytokine mediated inflammation
- CD8: direct cytotoxicity

101
Q

Many chronic inflammatory diseases are what type of hypersensitivity?

A

IV: T cell mediated

102
Q

Describe type IV CD4 mediated hypersensitivity

A
  • cytokines induce inflammation –> tissue destruction
  • delayed-type: 48-72 hrs
  • most Th1, some Th17
103
Q

Describe type IV CD8 mediated hypersensitivity

A
  • kill antigen-expressing target cell
  • effective in virus infected cells (MHC1)
104
Q

T/F type IV hypersensitivity rxn require secondary exposure?

A

true

105
Q

What are examples of T cell mediated diseases?

A
  • Rheumatoid arthritis
  • multiple sclerosis
  • Type I diabetes mellitus
  • IBD
  • psoriasis
  • contact sensitivity
106
Q

Describe Type I diabetes mellitus.

A
  • cytotoxic T cells target & destroy antigens of pancreatic islet B cells
107
Q

Describe contact sensitivity

A
  • various environmental chemicals stimulate inflammation mediated by Th1 cytokines –> skin blisters & rash
108
Q

Describe primary immunodeficiency syndromes.

A
  • detected in infancy (6mo-2yrs)
  • affect innate or adaptive
  • most involve B & T lymphocytes
109
Q

What causes primary immunodeficiency syndromes?

A

defects in checkpoints of B & T cell development

110
Q

What type of syndrome is SCID?

A

primary immunodeficiency
– severe combined immunodeficiency

111
Q

What is SCID?

A
  • many genetically distinct syndromes with defects cell mediated & humoral immunity
  • susceptible to severe recurrent infections
  • death in first year without stem cell transplantation
112
Q

What is Digeorge syndrome?

A
  • primary immunodeficiency
  • deletion on chromosome 22
  • congenital defect in thymic development
  • vulnerable to viral, fungal, & protozoal infections
113
Q

Features of digeorge syndrome?

A

CATCH 22
- cardiac abnormality
- abnormal facies
- thymic aplasia
- cleft palate
- hypocalcemia/hypoparathyroidism
*chromosome 22 deletion

114
Q

What is Hyper-IgM syndrome?

A
  • primary immunodeficiency
  • inability of T cells to activate B cells
  • normal to high levels IgM antibody
  • decreased: IgG, IgE, IgA
  • recurrent pyogenic infections, susceptible to pneumonia
115
Q

Why can’t T cells activate B cells in hyper IgM syndrome?

A

lack of class switching due to disruption of CD40 ligand

116
Q

Primary immunodeficiencies that affect innate immunity?

A
  • LAD
  • Chediak Higashi
  • complement function (C2 deficient)
117
Q

What are complications with chediak higashi syndrome?

A
  • defective platelets –> bruise/bleeding
  • melanocyte abnormality–> albinism
  • nervous system –> peripheral neuropathy
118
Q

Are primary or secondary immunodeficiencies more common?

A

secondary

119
Q

Secondary immunodeficiencies are encountered in what individuals?

A
  • cancer
  • diabetes
  • chronic infection
  • chemo/radiation therapy
  • immunosuppressants meds
120
Q

What is AIDS?

A
  • acquired immunodeficiency syndrome
  • HIV – ssRNA virus
  • transmitted by blood or body fluids
  • > 75% sexual, parenteral, perinatal
121
Q

What is the pathogenesis of AIDS/HIV?

A
  • targets CD4 T cells
  • RT enzyme –> complementary DNA
  • integrates into host genome
  • cell death & release of virus or latency
    *antibodies develop, but not protective
122
Q

Life cycle sequence of HIV?

A
  • binds CD4 T cell
  • fusion
  • reverse transcriptase
  • integration
  • replication
  • assembly
  • budding
123
Q

Clinical features of HIV/AIDS?

A
  • asymptomatic
  • acute retroviral syndrome (50-70%)
    –> 1-6 wks post exposure
    –> extremely infectious (viremia)
    –> oral: erythema & ulceration
    –> lymphadenopathy, sore throat, fever, headache, my/arthralgia, diarrhea, photophobia, peripheral neuropathies
  • latency: several mo-15yrs
124
Q

Progression of HIV/AIDS is affected by what factors?

A
  • age
  • immune response
  • treatment
125
Q

How to diagnose AIDS?

A

CD4 declines 200 cells/mm3
CD4 <14% total lymphocytes

126
Q

What are a few AIDS defining conditions?

A
  • candidiasis
  • herpes simplex
  • kaposi sarcoma
  • lymphoma
  • pneumonia
127
Q

HIV treatment?

A
  • anti-retroviral therapy (ART) decreases replication of virus
    –> reduce viremia: reduce risk of transmission, death, and transition to AIDS
128
Q

What are the classes of antiretroviral therapy?

A
  • nucleoside reverse transcriptase inhibitor –> incorporates into host DNA to inhibit replication
  • non-nucleoside reverse transcriptase inhibitor –> directly inhibits RT
  • protease inhibitors
  • fusion inhibitors
  • integrase inhibitors
  • CCR5 inhibitors

Pathology (9 decks)

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