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SPM > Week 10 > Flashcards

Week 10 Flashcards

1
Q

Define Humoral Immunity and what is it activated by.

A
  • Humoral immunity: antibody responses that act to inactivate microorganisms
    • Activated by both T-helper cells and microorganisms themselves (+ products)
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2
Q

What are the two ways that B-Cell Activation occurs and what are the activation stages??

A
  • T-dependent pathway (shown in picture)
  • T-independent pathway
  • Activation Stages
    • Contact and regcognition of microorganism
    • Activations signals through BCR via T-helper
    • Antibody Secretion
    • Isotype Switching
    • Affinity Maturation
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3
Q

What is the antigen receptor-mediated signal transduction in B lymphocytes?

  • What transcription factors are activated?
A
  • Signal transduction activated via phosphorylation of Ig-alpha and Ig-beta – co-stimulatory motifs
  • Phorsphorylation cascade leads to activation of transcription factors: Myc, NFAT, NF-(kappa)B, and AP-1
  • B-cells can also be activated via toll-like receptors (TLRs) or the complement pathway
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4
Q

What are the five consequences of Ig-mediated B-cell activation?

A
  • Clonal expansion
  • Ability to respond to cytokines produced by helper T cells
  • Interaction with helper T cells
  • Migration from follicle to T-Cell zone
  • Early phase of humoral immune response via secretion of ABs
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5
Q

Define isotype in terms of B-cells.

  • What process allows for the production of isotypes?
  • What is the chain order?
A
  • Isotype: heavy chain variations of Igs
    • Happens via class-switching, which is regulated by CD40/CD40L
    • Chain Order: VDJ – MDGEA (aka Dr. Gea)
    • VDJ hypermutations are conserved during class-switching so antigen specificity is preserved
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6
Q

Define affinity maturation and what enzyme catalyzes this process?

A
  • Affinity maturation: random hypermutations that lead to stronger affinity against antigens via AID
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7
Q

Define plasma cell, in terms of B-Cells.

A
  • Plasma cell: B-cells that act as antibody secreting factories
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8
Q

For T-dependent antigens:

  • Primary or secondary response?
  • What do they recognize?
  • Does affinity maturation occur?
  • Are they short-lived or long lived?
  • Class switching and hypermutation?
A
  • T-dependent antigens
    • Secondary response
    • Recognizes proteins (linear epitope)
    • B-cell acts like APC to create peptide + MHC Class II
    • T-helper cell recognizes peptide + MHC Class II and activates B-cell somatic hypermutations and class-switching
    • Affinity maturation (see board drawing)
    • Long-lived
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9
Q

For T-independent antigens:

  • Primary or secondary response?
  • What do they recognize?
  • Does affinity maturation occur?
  • Are they short-lived or long lived?
  • Class switching and hypermutation?
A
  • T-independent antigens
    • Primary response
    • Recognizes polymeric structures (conformational epitope)
    • No need for T-cell activation process – only IgM antibodies produced to label organisms for degradation
    • No affinity maturation (see board drawing)
    • No class switching/hypermutation
    • Short-lived
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10
Q

For Primary B-cell response:

  • Is it the first exposure or second exposure?
  • Is it slower or faster than secondary?
  • Is it facilitated via T-dependent or T-independent?
  • What B-cells does it utilize?
A
  • Primary B-cell response
    • First exposure to microorganism/antigen
    • Slower, less specific, and in smaller magnitude than 2º
    • T-independent response (mainly IgM)
    • Utilizes marginal B-cells (in lymph tissue) and B-1 B-cells (in periphery)
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11
Q

For Secondary B-cell response:

  • Is it the first exposure or second exposure?
  • Is it slower or faster than primary?
  • Is it facilitated via T-dependent or T-independent?
  • What B-cells does it utilize?
A
  • Secondary B-cell response (recall response)
    • Second exposure to microorganism/antigen
    • Faster, more specific, and in greater magnitude due to memory B-cells from 1º
    • T-dependent response (increase in IgG and other class-switches)
    • Utilizes follicular B-cells (undergo class-switching in germinal centers of lymph nodes)
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12
Q

How does negative feedback of B-cells occur?

  • What cells facilitate this process?
  • What cytokines are released by this cell?
A
  • Negative feedback
    • T regulatory cells release cytokines that deactivate all lymphocytes
    • Cytokine released: IL-10 by T-cells activates ITIM, which blocks signal transduction
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13
Q

What are the 3 clinical outcomes of patients with B-cell abnormalities?

A
  • Three clinical outcomes of patients with B-cell abnormalities
    • Defect in B-cell development
    • Excess IgA production
    • X-linked hyper IgM
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14
Q

What are the three mechanisms used by secreted antibodies to combat infections?

A
  • Neutralization of microbes/toxins
  • Opsonization and phagocytosis
  • Antibody-dependent cellular cytotoxicity
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15
Q

What are the 4 isotypes of antibodies and what are their functions?

A
  • IgG – neutralizes microbes (too big to enter epithelial barrier) and toxins (prevents engagement with receptors) and triggers opsonization
  • IgM – activates classical complement pathway
  • IgA – mucosal immunity
  • IgE – eosinophil- and mast cell-mediated defense against helminths; allergy
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16
Q

What is the role of these complement pathway proteins?

  • C3b
  • C5b6789
  • C5a
  • C3a, C4a, C5a
A
  • C3b activates macrophages for phagocytosis and opsonization (ROS – NADPH Burst)
  • Membrane attack complex (C5b6789) triggers cell lysis by puncturing plasma membrane
  • C5a is a chemokine that attracts macrophages and neutrophils to site of infection (follows gradient)
  • C3a, C4a, C5a activates basophils and mast cells to release histamine and serotonin → inflammatory response
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17
Q

Define opsonization and how does this process occur?

  • What receptors are required and what do they bind to?
A
  • Opsonization – antibody-mediated phagocytosis that leads to NADPH Burst
    • Fc Receptors (FcRs) bind Fc component of ABs to induce pathway
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18
Q

Define phagocytosis and how does it occur:

  • What receptor is needed and what does it bind to?
A

actin-mediated engulfs foreign objects

  • Fc receptor – binds Fc component of AB leading to phagocytosis or activation of cell
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19
Q

What is the alternate pathway and how is it initiated?

A
  • Alternative pathway
    • Initiated via C3 convertase formation in addition to Factor B and D binding
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20
Q

What is the classical pathway initiated by?

A
  • Classical pathway
    • Initiated via antigen-antibody binding
    • C1 binds to antibody at the Fc region
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21
Q

What is the lectin pathway initiated by?

A
  • Lectin pathway
    • Initiated via lectin binding mannose residues on foreign cells
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22
Q

How is mucosal immunity facilitated?

A
  • IgA transport across epithelial barrier to lumen
    • IgA dimerizes via linker J chain
    • Once secreted into lumen, it binds antigens to inactivate microbes.
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23
Q

What are three mechanisms of evasion of humoral immunity by microbes?

A
  • Antigenic variation – mutation of antigen-specific sites or variants of surface proteins
  • Inhibition of complement pathway – complement-binding proteins expressed by bacteria
  • Cell-surface structure for blocking – structures that prevent antibodies from binding (i.e. hyaluronic acid capsules)
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24
Q

What are the 5 vaccination types and what are their forms of protection?

A
  • Attenuated pathogens
    • Antibody response
  • Subunit vaccines
    • Antibody response
  • Conjugate vaccines
    • Helper T – Cell dependent antibody response
  • Synthetic vaccines
    • Antibody Response
  • Recombinant viruses and bacteria
    • Cell-mediated and humoral immune responses
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25
Q

What is paroxysmal nocturnal hemoglobinuria?

A
  • complement-mediated intravascular RBC lysis
  • patients may report red or pink urine (from hemoglobinuria)
  • Treatment: eculizumab (terminal complement

inhibitor)

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26
Q

Early defects in the complement system predispose a patient to:

A

ICX (immune complex) disease

  • Example: Depressed C3 is seen in active Lupus (SLE)
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27
Q

Late defects in the complement pathway predispose to:

A
  • Predisposition to Neisseria
    • Types of Neisseria
      • Meningococcal Meningitis
    • Defects in Complement Pathway
      • C5b, C6, C7, C8, C9 (any component in MAC)
    • Patients with these defects often have reoccurrences because they are unable to use complement pathways to lyse bacteria
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28
Q

What type of vaccinations are used to prevent infections? List three vaccines.

A
  • Bacterial vaccines must be used to prevent infections
    • Haemophilus influenzae, pneumococcal, meningococcal
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29
Q

A depressed alternative pathway predisposes to:

A
  • Sepsis
    • Defects in C3 ALSO predispose to sepsis
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30
Q

For Hereditary Angioedema (HAE),

  • What is the Etiology?
  • A decrease in what complement protein is seen?
  • What sympyoms are seen?
  • What is the pathophysiology?
  • What is the treatment?
A
  • HAE
    • Etiology: decreased C1esterase inhibitor
    • Diagnosis: depressed C4 levels
    • Systemic swelling
    • Contact Pathway: Factor 12 →→→→ bradykinin (all steps are inhibited by C1esterase Inhibitor)
      • Increase in bradykinin → vasculature permeability (NO and PGI2) → angioedema
    • Treatment: C1esterase Inhibitor
      • Epinephrine can only be used histamine-induced angioedema
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31
Q

What is the best test for assessing a classical complement deficiency?

  • What will the level of this test be if a complement protein is absent?
A
  • CH50 Test
    • If a complement component is absent, the CH50 level will be zero; if one or more components of the classical pathway are decreased, the CH50 will be decreased because lysis in the assay will not occur
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32
Q

Primary Immunodeficiencies

4 classes

A
  1. Phagocyte dsyfunction
  2. B-cell Disorders
  3. T-cell Disorder
  4. B and T cell Disorders
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33
Q

Defects in Phagocyte Dsyfunction

3 Types

A
  1. Chronic Granulomatous Disease
  2. Leukocyte Adhesion Defects (LAD)
  3. Chediack-Higashi Syndrome
34
Q

Defects in B Cell Development and Function

3 Types

A
  1. X-Linked Gamma Agammaglobulinemia
  2. Selective IgA Deficiency
  3. Common Variable Immunodeficiency (CVID)
35
Q

Defects in T Cell Development and Function

2 Types

A
  1. DiGeorge syndrome
  2. Hyper IgE
36
Q

Defects in T and B Cell Development and Function

4 Types

A
  1. Wiskott-Aldrich Syndrome
  2. Hyper-IgM Syndromes
  3. SCID
  4. Ataxia-Telangiectasia
37
Q

Secondary (Acquired) Immunodeficiency

One example.

A

HIV/AIDS

38
Q

Chronic Granulomatous Disease

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

Diagnosis

A
  • Etiology: mutations in phagocyte oxidase (NADPH Burst)
  • Pathophysiology: inability to kill phagocytosed microbes
  • Symptoms: recurrent infections
  • Diagnosis: NBT Tests (histological view of macrophage activity)
39
Q

Leukocyte Adhesion Defects (LAD) (3 types)

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Overall pathophysiology: failure to recruit leukocytes to sites of infection
  • Symptoms: leukocytosis and recurrent infections early in life
  • Types
    • Type I
      • Etiology: mutation in CD18 gene → defect in integrin
      • Diagnostic characteristics: delayed umbilical cord separation
    • Type II
      • Etiology: abnormality in fucosylation (glycosylation of sialyl Lewis X) → defect in sialyl Lewis X → required for leukocyte-endothelium binding
      • Diagnostic characteristics: severe mental/growth retardation
    • Type III
      • Etiology: mutation in KINDLIN-3 gene → defective platelet aggregation
      • Diagnostic characteristic: excessive bleeding
40
Q

Chediack-Higashi Syndrome

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutation in LYST gene
  • Pathophysiology: defective phagosome-lysosome fusion
  • Symptoms: recurrent infections and giant lysosomes in leukocytes
  • Diagnostic characteristic: albinism
41
Q

Defects in TLR Pathways

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • TLR3 mutations →→ herpes simplex encephalitis
  • NEMO (NF-kB Essential Modulator) → ectoderm defects → lack of sweating
42
Q

Severe Combined Immunodeficiencies (SCID)

(4 Types)

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Pathophysiology: impaired T cell development with or without impaired B cell or NK cell development
  • Symptoms:
    • Infections by live attenuated vaccines (chicken pox, MMR)
    • Skin rash via maternal graft (graft-versus-host reaction)
  • Diagnosis: TREC Assay (absence of TREC = absence of T cells = SCID)
  • Types
    • DiGeorge Syndrome
      • Etiology: 22q11 deletion
      • Diagnostic characteristics: defective parathyroid glands/thymus and facial deformities
    • ADA Deficiency (adenosine deaminase)
      • Etiology: mutation in adenosine deaminase (purine salvage pathway)
      • Diagnostic characteristics: reduction of lymphocyte numbers
    • X-linked SCID
      • Etiology: mutations in interleukins
    • Absence of V(D)J Recombination
      • Etiology: mutations in NHEJ pathway → lack of specificity for epitopes
43
Q

X-Linked Gamma Agammaglobulinemia

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutations in Bruton Tyrosine Kinase
  • Pathophysiology: failure of B cell maturation past pre-B
  • Diagnostic characteristic: no germinal centers in lymph nodes
44
Q

Selective IgA Deficiency

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Pathophysiology: IgA deficiency (important in mucosal regions)
  • Symptoms: increased incidence of respiratory and GI infections
45
Q

Common Variable Immunodeficiency (CVID)

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Pathophysiology: low IgG, IgA, IgM
  • Diagnostic characteristics: low IgG leads to impaired antibody response to vaccines
46
Q

X-Linked Hyper-IgM Syndrome

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutations in CD40L (CD154) gene
  • Pathophysiology: defect in class-switching; low levels of all Igs except IgM
  • Symptoms: severe and frequent infections
47
Q

Wiskott-Aldrich Syndrome

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutation in WASP
  • Pathophysiology: decreased actin polymerization in cytoskeleton
  • Symptoms: skin bleeding
48
Q

Hyper-IgE Syndromes (HIES)

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: dominant negative mutation in STAT3 or recessive mutation in DOCK8
  • Symptoms: eczema, eosinophilia, two rows of teeth
49
Q

X-Linked Lymphoproliferative

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutation in SLAM, SAP, or XIAP
  • Pathophysiology: decreased NK and T cell activation
  • Diagnostic characteristics: inability Epstein-Barr virus (EBV)
50
Q

Ataxia-Telangiectasia

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: defect in ATM (DNA repair protein)
  • Symptoms: abnormal gait and neurological deficits
51
Q

HIV

Etiology

Pathophysiology

Symptoms

A
  • Etiology: virus that interacts with chemokine receptors of CD4+ T Cells
  • Pathophysiology: reduction of CD4+ T cell counts
    • Acute Phase: momentary spike in viral load and reduction of CD4+ cells
    • Chronic Phase: clinical latency and asymptomatic
    • AIDs: CD4+ cells less than 200 cells/mm3
  • Symptoms: tumors and opportunistic infections
52
Q

Recognize the signs and symptoms of clinical anaphylaxis.

A
  • Constitutional Symptoms
    • Urticaria (hives), angioedema (swelling)
  • Eyes
    • Red, watery eyes
  • ENT
    • Bluish lips, runny nose
  • Cardio
    • Increased HR, vasodilation
  • Respiratory
    • Shortness of breath, wheezing
  • Neuro
    • Altered mental status, sense of doom, fainting
  • GI
    • Abdominal pain, vomiting, diarrhea
53
Q

Explain the pathophysiology of an anaphylaxis event.

A

Type I Reaction Sensitization (onset is seconds to minutes)

Allergen → APC → TH2 cell → activates B Cell → IgE ABs → activates mast cells/basophils → mast cell degranulation → release of histamines, cytokines, leukotrienes, prostaglandins

Food allergy causes this response, but food intolerance just causes pain with no antibody response

54
Q

Relate the leukotriene and prostaglandin pathway to hypersensitivity reactions.

Explian each normal pathway and the end result of each pathway..

A
  • PM FAs → arachidonic acid → PGH2 → PGE2 → PGE2 binds to EP-Rs on mast cells and eosinophils → inhibits inflammatory response
    • COX1/COX2 are needed for AA to PGH2
  • PM FAs → arachidonic acid → LTX4 (variants of leukotrienes) → inflammation
55
Q

What happens in AERD?

A

Aspirin Exacerbated Respiratory Disease (AERD)

  • If you take aspirin, you get COX blocks → inhibition of PGE2 → increased release of LTs from mast cells → increased inflammatory response
  • Diagnostic characteristics: acute dyspnea, nasal polyps and nasal inflammation
  • Treatment: aspirin desensitization and “–lukast” drugs (leukotriene modifiers)
56
Q

Identify treatment strategies for anaphylaxis.

A

Intermuscular injection of epinephrine

Acute symptoms: antihistamines

57
Q

In central T lymphocyte tolerance, when an immature T cell has high affinity for self-antigens, two things can happen:

A
  • Negative selection → deletion
  • Development of regulatory T cell → suppression
58
Q

In central B cell tolerance (bone marrow), when immature B cell has high affinity for self-antigens, three things can happen:

A
  • Receptor editing: re-expression of recombinase to create new Ig light chains
  • Apoptosis: deletion
  • Anergic B cell
59
Q

In peripheral T lymphocyte tolerance, when a mature T cell has high affinity for self-antigens,

  • What three things can happen?
  • What are the way each of these three things happen?
A
  • Anergy → unresponsive T cell due to
    • Signaling block: no co-stimulation
    • Binding of inhibitory receptor (PD-L1)
  • Suppression by Regulatory T cells
    • CD4+ cells that express CD25 and FoxP3 (TFs)
    • Secrete IL-10 and TGF-B
    • Competes for IL-2
  • Apoptosis → deletion
    • Via intrinsic signals (with no co-stimulation)
    • Via death receptors (FasR)
60
Q

In peripheral B cell tolerance, when a mature B cell has high affinity for self-antigens,

  • What three things can happen?
  • What are the ways that these happen?
A
  • Anergy → no co-stimulation with CD40
  • Apoptosis → deletion
  • Regulation by inhibitory receptors
61
Q

What gene is mutated in IPEX and what is the result of this mutation?

A

FoxP3 mutation → few to no Tregs produced → increased immune activity

62
Q

What genes have mutations in Autoimmune Lymphoproliferative Syndrome?

A

Mutations in genes associated with apoptosis (caspases, Fas)

63
Q

What is the difference between an antigen and immunogen?

A
  • Antigen: any substance recognized by AB or T cell
  • Immunogen: antigen capable of eliciting response (all antigens are not immunogens)
64
Q
  • What is a live, attenuated vaccine?
  • Do they require a booster?
  • What are some examples of this?
A
  • Infectious agents have reduced virulence due to mutations or genetic engineering
  • Give strongest response and longest protection
  • Examples: MMR, chickenpox
65
Q
  • What is an inactivated vaccine?
  • Do they require boosters?
  • What is an example?
A
  • Infectious agents have been killed by fixatives or chemicals so they cannot produce proteins or replicate in cells
  • Requires boosters
  • Safer than attenuated
  • Examples: seasonal influenza vaccines
66
Q
  • What are subunit vaccines?
  • Do they require boosters?
  • What are two examples?
A
  • Contain only a “subunit” or portion of an organism
  • Requires boosters
  • HPV and HepB
67
Q
  • What are conjugate vaccines?
  • Do they require a booster?
  • What are some examples?
A
  • Vaccine against encapsulated bacteria – conjugates polysaccharide + protein carrier (protein carrier is needed to act as peptide in MHC complex because when bacteria is broken down, this protein subunit can be used as peptide)
  • Safe because it lacks infectious agent
  • Examples: Neisseria meningitidis, H. flu, and streptococcus pneumoniae
68
Q
  • What is the role of adjuvants in the success of vaccines?
  • What do they activate?
  • What are some examples?
A
  • Adjuvant: any substance that enhances the immune response to an antigen with which it is mixed
    • Aluminum salts/gels
    • Monophosphoryl lipid A
  • Activate PRRs (TLRs, NODs)
69
Q

Herd immunity and neutralization are two immune mechanisms that provide protection after vaccination. How does each work?

A
  • Herd immunity: if most of the population is vaccinated, infections do not spread
  • Neutralization
    • Neutralizing antibodies: binding prevents infections
    • Non-neutralizing antibodies: binding does not prevent infection
    • Broadly neutralizing antibodies: recognize a non-specific epitope found in multiple subtypes of a pathogen; the antibody can undergo hyper-mutation to become more specific to each pathogen with time
70
Q
  • What is a type A drug reaction?
  • Is it predictable?
  • What is it dependent on?
  • How common are these?
A
  • Most adverse reactions
  • Predictable – related to the pharmacological action of drug
  • Dose dependent
71
Q
  • What is a type B reaction?
  • Is it predictable?
  • How common are they?
  • What are three types of type B reactions?
A
  • Unpredictable – unrelated to known pharmacological action of drugs
  • Types of type B reaction
    • Intolerance – known side effect at lower dose than expected
    • Idiosyncratic – based on how patient metabolizes drug
    • Hypersensitivity/allergy/immune mechanisms
72
Q

What is the diagnostic test for a type I hypersensitivity reaction?

A

skin testing

73
Q

What is the diagnostic test for a type II hypersensitivity reaction?

A

blood smear for hemolysis

74
Q

What is the diagnostic test for a type III hypersensitivity reaction?

A

check for equal AB/antigen ratio

75
Q

What is the diagnostic test for a type IV hypersensitivity reaction?

A

CBC

76
Q
  • What happens in a type I hypersensitivity reaction?
  • What are some common clinical characteristics?
  • What activates this response?
  • What effector cells respond?
  • What are examples of this reaction?
A
77
Q

What happens in a type II hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

A
78
Q

What happens in a type III hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

A
79
Q

What happens in a type IVa hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

A
80
Q

What happens in a type IVb hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

A
81
Q

What happens in a type IVc hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

A
82
Q

What happens in a type IVd hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

A

SPM (17 decks)

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