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Immunology Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the three functions of lymph nodes?

A
  1. Non-specific filtration by macrophages
  2. Storage of T and B cells
  3. Immune response activation
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2
Q

What are the histo-anatomical components of a lymph node?

A

Each node has an afferent and efferent lymphatics and vessels. A central medullary sinus is fed by medullary cords containing reticular cells and macrophages. The periphery is made up of follicles containing B cells and germinal centres, and the paracortex, made up of T cells.

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3
Q

What are the haematological sequelae post splenectomy?

A

Howell-Jolly bodies
Target cells
Thrombocytosis
Lymphocytosis

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4
Q

Thymomas are associated with?

The thymus is hypoplastic in?

A

Myasthenia gravis and SVC syndrome.

Hypoplastic in DiGeorge and SCID.

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5
Q

What are the diseases associated with HLA-B27?

A 
(P.A.I.R)
Psoriatic arthritis
Ankylosing spondylitis
IBD-associated arthritis
Reactive arthritis
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6
Q

Which HLA subtype is associated with Coeliac Disease?

A

(I 8 2 much gluten at Dairy Queen)

DQ8 and DQ2

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7
Q

Which diseases are associated with HLA subtype DR2?

A

(Multiple hay pastures have dirt)

Multiple sclerosis
Hay fever
SLE (also HLA-DR3)
Goodpasture syndrome

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8
Q

What are the MHC I loci?

What are the MHC II loci?

A

MHC I loci have 1 letter: HLA-A, HLA-B, and HLA-C

MHC II loci have 2 letters: HLA-DP, HLA-DQ, HLA-DR

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8
Q

What does MHC I bind to?

What does MHC II bind to?

A

Both bind to TCR

MHC I binds to CD8 - presents to CD8+ cytotoxic T cells
MHC II binds to CD4 - presents to CD4+ helper T cells

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9
Q

What is the difference in antigen presentation between MHC I and II complexes?

A

MHC I present endogenously synthesized antigens which are loaded via the RER after divert via a TAP. Found in all nucleated cells, APC and platelets

MHC II present exogenously synthesized antigens following release of “invariant chain” in an acidified endosome. Found only on MHC.

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10
Q

What are Natural Killer cells?

How do they kill?

A

NK cells are lymphocyte members of the innate immune system.

They use perforin and granzymes to induce apoptosis of virally infected cells and tumour cells.

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11
Q

What are the two ways NK cells are induced to kill?

A
  1. When exposed to a non-specific activation target and/or an absence of MHC I on the target cell
  2. Via antibody-dependent cell-medicated cytotoxicity (CD16 bonds to Fc region of Ig)
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12
Q

Describe the process of T Cell differentiation:

A

T cell precursors migrate from the bone marrow to the Thymus, where they undergo positive selection (TCR/CD4/CD8) in the cortex. They then undergo negative selection (against self-antigens) in the medulla where they are split between Cytotoxic T cells and Helper T cells.

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13
Q

What are the 4 types of Helper T cell?

A

Th1
Th2
Th17
Treg

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14
Q

Which cytokines promote and inhibit differentiation of Th1 from the Helper T cell population?

A

+ IL-12, IFN-y

  • IL-4, IL-10
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15
Q

Which cytokines promote and inhibit differentiation of Th2 cells from the Helper T cell population?

A

+ IL-2, IL-4

  • IFN-y
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16
Q

What do Th1 cells do?

Which cytokines do they secrete?

A

Th1 cells activate macrophages and cytotoxic T cells.

They secrete IFN-y and IL-2

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17
Q

What do Th2 cells do?

Which cytokines do they secrete?

A

Th2 cells recruit eosinophils for parasite defence and promote IgE production by B cells.

They secrete IL-4, IL-5, IL-6, IL-10, and IL-13

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18
Q

What is the macrophage-lymphocyte interaction?

A

Dendritic cells, macrophages and other APCs release Il-12, which stimulates T cells to differentiate into Th1 cells, which release IFN-y, which stimulates macrophages.

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19
Q

What are regulatory T cells?

What are their CD markers?

A

Treg cells help maintain specific immune tolerance by suppressing CD4 and CD8 T cell effector functions. They produce the anti-inflammatory cytokines (IL-10 and TGF-B).

They express CD3, CD4, CD23, and FOXP3j

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20
Q

What is IPEX?

A

Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked syndrome.

Genetic deficiency of FOXP3.

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21
Q

Describe the 4-stage process of T cell activation:

A
  1. Dendritic cell samples antigen, migrates to lymph node
  2. Antigen is presented on MHCI/II and recognised by CD4/8
  3. Costimulatory signal via interaction of B7 protein on dendritic cell and CD28 on naive T cell
  4. Th cell activates and produces cytokines.
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22
Q

Describe the 4-stage process of B cell activation/class switching:

A
  1. Th cells activation as above
  2. B-cell receptor mediated endocytosis; foreign antigen is presented on B cell MHC II and recognised by TCR on Th cell
  3. CD40 receptor on B cell binds to CD40L on Th cell
  4. Th cell secretes cytokines that determine Ig class switching of B cell.
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23
Q

What is the Fab region of an antibody?

A

The fragment, antigen binding region.

The Fab determines idiotype; only one antigenic specificity expressed per B cell.

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24
Q

What is the Fc region of an antibody?

A

The fragment, constant. It determines isotype (IgM, IgA, etc)

This is a Constant, Carboxy terminal, with Carbohydrate side chains, that is Complement binding.

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25
Q

How is antibody diversity generated?

A
  1. Random recombination of V(D)J light(heavy) chain genes
  2. Random combination of Heavy chains and Light chains
  3. Random addition of nucleotides to DNA during recombination by terminal deoxynucleotidyl transferase.
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26
Q

How is antibody specificity generated?

A
  1. Somatic hyper mutation and affinity maturation (variable region)
  2. Isotype switching (constant region)
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27
Q 
Which Ig isotype:
Crosses the placenta?
Is the most abundant?
Is the least abundant?
Is the immediate responder?
Is the delayed responder?
Is a pentamer?
Is a dimer?
A

IgG crosses the placenta and is the most abundant.
IGE has the lowest concentration in plasma.
IgM is the immediate responder.
IgG is the delayed responder.
IgM is a pentamer (big so can’t cross placenta).
IgA is a dimer.

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28
Q

What are Thymus-independent antigens?

What is their importance?

A

Thymus independent antigens are antigens lacking a peptide or protein component (eg LPS from G-bacteria). These cannot be presented by MHC to T cells and are therefore weakly immunogenic. These antigen vaccines often require boosters and adjuvants.

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29
Q

Which cytokine is the predominant inducer of the acute phase reactants (CRP, Ferritin, Fibrinogen, Hepcidin, Serum amyloid A)?

A

IL-6

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30
Q

What are the three pathways by which the complement cascade may be activated?

A
  1. The classic pathway (IgG or IgM)
  2. The alternative pathway (microbe surface molecules)
  3. The Lectin pathway (mannose/other sugars on microbe surface)
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31
Q 
What are the roles of:
C3b?
C3a, C4a, C5a?
C5a?
C5-C9?
A

C3b - Opsonization (along with IgG)
C3a, C4a, C5a - anaphylaxis
C5a - neutrophil chemotaxis
C5-C9 - cytolysis by the MAC.

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32
Q

What are the inhibitors of the complement system?

What diseases result from their deficiency?

A

CD55 or Decay-Accelerating Factor.
C1 esterase.

CD55 deficiency causes lysis of RBCs and PNH
C1 esterase deficiency causes hereditary angioedema due to unregulated activation of kallikrein.

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33
Q

What are the roles of interleukins 1-6?

A

“Hot T-bone stEAK”

IL-1 causes fever
IL-2 stimulates T cells
IL-3 stimulates bone marrow
IL-4 stimulates IgE
IL-5 stimulates IgA 
IL-6 stimulates aKute phase reactants.
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34
Q

What are the roles of TNF-a?

A

Activates endothelium, causes WCC recruitment, vascular leak.

Causes cachexia in malignancy and maintains granulomas in TB.

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35
Q

Which interleukins mediate sepsis?

A

IL-1 fever
IL-6 acute phase reactants
TNF-a vascular leak, leucocytosis.

36
Q

What is the role of IFN-y? What secretes it?

A

Secreted by NK cells and T cells in response to antigen or IL-12 from macrophages. Stimulates macrophages to kill phagocytosed pathogens. Also activates NK cells to kill virus infected cells. Increases MHC expression.

37
Q

What are the lymphocyte coreceptors for HIV?

A

CXCR4 and CXCR5.

38
Q

What is the B-cell receptor for EBV?

A

CD21

39
Q

How do super antigens from S. pyogenes and S. aureus cause such massive cytokine release?

A

They cross link the beta region of the TCR to the MHC II on APCs, so that any T cell can be activated. i.e not restricted to the clonal T cell specific for the antigen.

40
Q

Which diseases can we treat with pre-formed antibodies?

A

“To Be Healed Very Rapidly” by passive immunisation.

Tetanus toxin
Botulinum toxin
HBV
Varicella
Rabies
41
Q

What is a live attenuated vaccine?

What examples are there?

A

LAVs contain organisms that lose their pathogenicity but retain the capacity for transient growth within the inoculated host. Induces a cellular and humoral response.

Examples include MMR, BCG, Polio, Rotavirus, and Yellow Fever.

42
Q

What is an inactivated or killed vaccine?

What are some examples?

A

The pathogen is inactivated by heat or chemicals. The maintained epitope structure allows for antigenic development of a humoral response.

Examples include Rabies, Influenza, Polio, and Hep A.

43
Q

What are the four types of Hypersensitivity reaction?

A

Type 1: Anaphylactic and Atopic
Type 2: Cytotoxic (antibody mediated)
Type 3: Immune complex mediated
Type 4: Delayed (cell mediated)

44
Q

Describe the pathophysiology of a Type 1 hypersensitivity reaction:

What are some examples?

A

Free antigen (eg dust) cross links IgE on pre-sensitised mast cells and basophils triggering immediate release of vasoactive amines that act at post capillary venues.

Examples include anaphylaxis and dust allergies.

45
Q

Describe the pathophysiology of Type 2 Hypersensitivity reactions:

What are some examples?

A

Antibodies bind to (self) cell-surface antigens and trigger destruction via opsonisation or cytotoxicity or inflammation via activation of the complement cascade. The process can also inhibit cellular function.

Examples include Autoimmune Haemolytic Anaemia, Transfusion reactions, Rheumatic fever, Myasthenia Gravis, Grave’s disease.

46
Q

Describe the pathophysiology of Type 3 Hypersensitivity reactions:

What are some examples?

A

Type 3 Hypersensitivity reactions are characterised by a pathological immune complex made up of an antigen, an antibody, and complement. This complex attracts neutrophils, which release lysosomal enzymes. Can be associated with vasculitis or systemic manifestations.

Examples include SLE, polyarteritis nodosa, and post-strep GN.

47
Q

Describe the pathophysiology of Type 4 Hypersensitivity reactions:

What are some examples?

A

Type 4 Hypersensitivity reactions do not involve antibodies (unlike Types 1,2, and 3). They are characterised by either direct CD8+ cytotoxicity against self, for example Type diabetes. Or delayed type hypersensitivity where sensitised CD4+ helper T cells encounter an antigen and release cytokines, for example contact dermatitis or graft versus host disease.

48
Q 
What are the autoantibodies for:
Myasthenia Gravis
Goodpasture syndrome
Antiphospholipid syndrome
CREST syndrome
A

Anti-Ach receptor
Anti-GBM
Anti-B2 glycoprotein
Anti-centromere

49
Q

What are the autoantibodies associated with Lupus?

Which are the most sensitive and specific?

A

Antinuclear antibodies (most sensitive)
Anti-dsDNA (specific and poor prognosis)
Anti-Smith or Anti-snRNPs (specific, not prognostic)
Antihistone antibodies (sensitive for drug induced SLE)

50
Q 
What are the autoantibodies for:
Scleroderma
Sjogren syndrome
Polymositis
Dermatomyostitis
A

Anti-Scl-70
Anti-SSA and Anti-SSB
Anti-synthetase (Anti-Jo-1)
Anti-helicase (Anti-Mi-2)

51
Q 
What are the autoantibodies associated with:
Primary biliary cirrhosis
Celiac disease
Autoimmune hepatitis
Pernicious anaemia
A

Anti-mitochondrial
IgA anti-endomysial and IgA anti-tissue transglutaminase
Anti-smooth muscle antibodies
Anti-parietal cell and anti-IF

52
Q

What is graft versus host disease?

A

GvH is an example of delayed-type Hypersensitivity (Type 4).

The condition occurs when competent T cells are transplanted into an immunocompromised patient and subsequently attack the recipient’s organs (skin, liver, GIT).

53
Q

What is Selective IgA deficiency?

A

Selective IgA deficiency is the most common primary immunodeficiency. Although most affected patients are asymptomatic, some have recurrent sinopulmonary and gastrointestinal infections due to absence of Secretory IgA.

Patients with severe IgA deficiency can form IgE antibodies to IgA. When given blood, they can develop fatal anaphylaxis.

55
Q

Describe the classification of immunodeficiency disorders:

A

B-cell disorders
T-cell disorders
B and T cell disorders
Phagocyte dysfunction disorders.

56
Q

List some of the more frequent B-cell immunodeficiency disorders:

A
  1. (X-linked) Bruton’s agammaglobulinaemia
  2. Selective IgA deficiency
  3. Common variable immunodeficiency.
57
Q

List some of the more common T-cell immunodeficiency disorders:

A
  1. Thymic aplasia (DiGeorge syndrome)
  2. IL-12 receptor deficiency
  3. AD Hyper-IgE syndrome
  4. Chronic mucocutaneous candidiasis.
58
Q

List the combined B and T cell immunodeficiency syndromes:

A
  1. Severe combined immunodeficiency
  2. Ataxia telangiectasia
  3. Hyper-IgM syndrome
  4. Wiskott-Aldridge syndrome
59
Q

List the immunodeficiencies caused by impaired phagocyte function:

A
  1. Leukocyte adhesion deficiency
  2. Chediak-Higashi syndrome
  3. Chronic granulomatous disease.
60
Q

What is the underlying defect in Bruton’s agammaglobulinaemia?

What is the classical presentation?

A

A defect in Bruton’s Tyrosine Kinase which is crucial for B-cell development.

Affected male infants classically present with recurrent bacterial and enteroviral infections after 6 months of age (maternal IgG). Resistance to viri and fungi (T cell mediated) is normal.

61
Q

What is the underlying defect in CVID?

What is the typical presentation?

A

Most common form of primary immunodeficiency but least well characterised. Ultimately a defect in B cell differentiation.

Affected individuals usually present after the age of 2 and may be considerably delayed. History of bronchiectasis, sinopulmonary infections, and increased risk of autoimmune disease and lymphoma.

62
Q

What is the pathophysiology of DiGeorge syndrome?

What is the classical presentation?

A

22q11 deletion; failure to develop 3rd and 4th pharyngeal pouches. Absent thymus and parathyroids.

Patients present with Tetany, T-cell deficiency, and Tetrology of Fallot and Truncus Arteriosus. T-cell deficiency results in recurrent viral and fungal infections.

63
Q

What is the classical presentation of an individual with IL-12 receptor deficiency?

A

Disseminated mycobacterium and fungal infections, may present after administration of BCG vaccine.

An impaired IL-12 receptor affects the function of Th1 cells and their production of IFN-y and subsequent activation of macrophages.

64
Q

What is Job syndrome?

How do affected patients present?

A

Job syndrome is an AD Hyper IgE syndrome.

Patients present with F.A.T.E.D:
Coarse Facies, cold Abscesses, retained Teeth, increased IgE, and Dermatological problems.

65
Q

What are the two main causes of Severe Combined Immunodeficiency?

A
  1. X-linked defective IL-2R gamma chain mutation

2. AR Adenosine deaminase deficiency

66
Q

What is the classical presentation of a patient with SCID?

A

Failure to thrive, chronic diarrhoea, thrush. Recurrent bacterial, fungal (B-cell), and viral and fungal (T-cell) infections.

67
Q

What is Ataxia-telangiectasia?

How is it clinically manifest?

A

A mixed B and T cell immunodeficiency due to a defect in the ATM gene, which results in failure of DNA ds break repairs.

It is manifest as a triad of Ataxia, spider Angiomas, and IgA deficiency. Patients are at increased risk of lymphoma and leukaemia.

68
Q

Describe the underlying defect in Hyper IgM syndrome:

What is the classical presentation?

A

Most commonly due to defective CD40L on Th cells. This results in a class switching defect. It is an X-linked recessive disorder.

Patients with Hyper IgM syndrome typically present with severe pyogenic infections early in life, often with opportunistic infections such as pneumocystis, cryptosporidium, and CMV.

69
Q

What is Wiskott-Aldridge syndrome?

What is the classical presentation?

A

Wiskott-Aldridge syndrome is an X-linked recessive syndrome caused by a mutation in the WASp gene which prevents leucocytosis and platelets from reorganising the actin cytoskeleton, which thereby causes defective antigen presentation.

The classical triad is that of (W.A.T.E.R):
Wiskott-Aldridge, Thrombocytopenia, Eczema, and Recurrent pyogenic infections.

70
Q

What is the underlying defect in Leucocyte Adhesion Deficiency?

What is the classical presentation?

A

LAD is caused by a defect in the LFA-1 integrin protein on phagocytes, which impairs migration and chemotaxis. It is autosomal recessive.

The classical presentation of recurrent infections of skin and mucosa is accompanied by absent pus and impaired wound healing. Delayed separation of the umbilical cord is often seen.

71
Q

What is the classical histological appearance in Chediak-Higashi syndrome?

What causes this?

A

Giant granules are seen in granulocytes and platelets.

This is because of a defect in Lysosomal Trafficking Regulator Gene (LYST). Phagosome-lysosome fusion is dysfunctional.

72
Q

What is the classical presentation of Chediak-Higashi syndrome?

A

Recurrent pyogenic infections by Staph and Strep. Partial albinism, peripheral neuropathy, progressive neurodegeneration, and infiltrative lymphohistiocytosis.

73
Q

What causes Chronic Granulomatous Disease?

What organisms are CGD patients more susceptible to?

A

CGD is caused by a defect in the the NADPH oxidase pathway. Usually autosomal recessive.

Patients with CGD have increased susceptibility to catalase positive organisms.

74
Q

How can CGD be diagnosed?

A

Abnormal dihydrorhodamine tests (reduced green fluorescence)

Nitroblue tetrazolium dye reduction tests fails (to turn blue).

75
Q

What are the time-frame, pathogenesis, and histological features seen in Hyperacute Transplant Rejection?

A

Within minutes.
Type II hypersensitivity, where pre-formed abs react to donor antigen.
Widespread thrombosis of graft vessels with ischaemia and necrosis.

76
Q

What are the time-frame, pathogenesis, and histological features seen in Acute Transplant Rejection?

A

Weeks to months.
Type IV hypersensitivity reaction where CD8+ T cells act against donor MHCs. Antibodies may develop after transplant.
Vasculitis with dense interstitial lymphocytic infiltrate.

77
Q

What are the time-frame, pathogenesis, and histological features seen in Chronic Transplant Rejection?

A

Months to years.
Type II and Type IV hypersensitivity. CD4+ T cells respond to recipient APCs presenting donor peptides. Both cellular and humoral responses occur.
Interstitial fibrosis with arteriosclerosis.

78
Q

How do Cyclosporine and Tacrolimus work?

What are their common side effects?

A

Both are calcineurin inhibitors that block T-cell activation by preventing IL-2 transcription.

Both are nephrotoxic. Unlike Cyclosporine, Tacrolimus does not give patients gingival hyperplasia or hirsutism. But it is diabetogenic.

79
Q

What is Sirolimus (Rapamycin)?

What are its common side effects?

A

mTOR inhibitor that binds FKBP which prevents the response of lymphocytes to IL-2.

Pan”sir”topenia but kidney “sir”vives. Also diabetogenic.

80
Q

What is Basiliximab?

A

A monoclonal antibody against IL-2.

81
Q

How does Azathioprine work as an Immunosuppressant?

What is the main side effect?

A

Azathioprine is an antimetabolite precursor of 6-mercaptopurine. It inhibits lymphocyte proliferation by blocking nucleotide synthesis.

It can cause pancytopenia.

82
Q

How does Mycophenolate mofetil work?

Why use it over/after other immunosuppressants?

A

Reversible inhibits IMP dehydrogenase in the purine metabolism, blocking synthesis of T and B cells.

It is less nephrotoxic and neurotoxic than others.

83
Q

What is Prednisone’s predominant mechanism of immunosuppression?

A

Corticosteroids inhibit NF-kb and therefore suppress lymphocyte function by reducing the transcription of many cytokines. It also induces T cell apoptosis.

84
Q

Sarcoidosis granulomas produce what?

A

Angiotensin converting enzyme
1,25-dihydroxycholecalciferol

Patients with sarcoidosis, therefore, will often have hypercalcaemia and a dry cough.

85
Q

What is Henoch-Schonlein purpura?

What is the pathogenesis?
What are the clinical manifestations?
How is the diagnosis confirmed?

A

HSP is an IgA immune-complex mediated vasculitis.
It typically follows a minor infection (URTI) and presents with palpable purpura, arthralgia, abdominal pain, and renal disease.
It can be diagnosed on skin biopsy showing IgA deposition in blood vessels.

86
Q

What is CD15 present on?

A

CD15 is a cell surface marker on granulocytes. It is also present on nearly all Reed-Sternberg cells and is therefore a useful cytological marker in HL.

87
Q

Where is CD16 found?

A

CD16 is a marker present on NK cells, neutrophils, and macrophages.

88
Q

What is CD15 present on?

A

CD15 is a cell surface marker on granulocytes. It is also present on nearly all Reed-Sternberg cells and is therefore a useful cytological marker in HL.

89
Q

Where is CD16 found?

A

CD16 is a marker present on NK cells, neutrophils, and macrophages.

USMLE (14 decks)

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