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Step 1 Subjects > Immunology > Flashcards

Immunology Flashcards

1
Q

Lymph node

A

Follicle= B-cells

  • Primary: dense, dormant
  • Secondary: pale, active

Medulla=

  • Cords: lymphocytes and plasma cells
  • Sinuses: reticular cells and macrophages; communicate with efferent lymphatics

Paracortex= T cells (between follicles and medulla)

  • Endothelial venules: B-cell entry from blood
    • Underdeveloped in DiGeorge syndrome
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2
Q

Lymph drainage

A

Rectum (above pectinate line): internal iliac

Anal canal (below pectinate line): superficial inguinal

Right lymphatic duct: drains right arm, right chest, right 1/2 of face
- Thoracic duct drains everything else

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3
Q

Sinusoids of spleen

A

Vascular channels in red pulp
- Fenestrated; macrophages nearby

White Pulp:

  • T cells= periarterial lymphatic sheath (PALS)
  • B cells= follicles

Macrophages remove encapsulated bacteria (IgM–> complement–> C3b opsonization–> macrophage removal)
- Strep pnumo, H. flu, N. meningitidis, Salmonella, Klebsiella, Strep agalactaciae (group B)

Post-splenectomy:

  • Howell-Jolly Bodies (nuclear remnants in RBCs)
  • Target cells (excess membrane: hemeglobin ratio)
  • Thrombocytosis
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4
Q

Thymus

A

Epithelium of 3rd branchial pouches

Cortex= dense, immature T cells
- Positive selection (MHC class restriction: T cells expressing TCRs binding self MHC)

Medulla= pale, mature T cells, Hassall’s corpuscles
- Negative selection (non-reactive to self antigens: high affinity for self–> apoptosis)

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5
Q

Innate immunity

A

Neutrophils, macrophages, dendritic cells, NK cells, complement

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6
Q

Adaptive immunity

A

Recognize pathogen–> V(D)J recombination

  • Slow response at first, memory faster
  • T cells, B cells, circulating antibody
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7
Q

MHC I

A

HLA-A, B, C

  1. Nucleated cell (any) infected with antigen
  2. Processed in RER (+ intracell peptides)
  3. Presented on MHC-I + Beta-2 microglob
  4. Binds TCR, CD8 T-cells

** Mediates viral immunity

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8
Q

MHC II

A

HLA-DR, HLA-DP, HLA-DQ

  1. Antigen presenting cell infected
  2. Antigen processed in acidic endosome
  3. Presented on MHC-II (peptide binding groove)
  4. Binds TCR, CD4 T-cells
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9
Q

HLA-A3

A

Hemochromatosis

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10
Q

HLA-B27

A

Psoriasis
Ankylosing Spondylitis
Inflammatory bowel disease
Reiter’s syndrome

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11
Q

HLA-DQ2/DQ8

A

Celiac disease

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12
Q

HLA-DR2

A

Multiple sclerosis
Hay fever
Systemic Lupus Erythematosis
Goodpasture’s disease

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13
Q

HLA-DR3

A

Diabetes Mellitus, Type 1

Grave’s disease

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14
Q

HLA-DR5

A

Pernicious anemia–> B12 deficiency

Hashimoto’s thyroiditis

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15
Q

Natural killer cells

A

Induce apoptosis of virally infected + tumor cells
- Only lymphocyte in innate immune system

Enhanced by IL-2, IL-12, IFN-beta, IFN-alpha

Kills target cell with:

  • Nonspecific activation signal
  • Absence of class I MHC
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16
Q

B-cell produced antibody functions

A

Type I hypersensitvity reaction: IgE produced (Allergy)

Type II reaction: IgG, IgM (Cytotoxic)

Type III reaction: IgG (immune complex)

** Hyperacute, humorally mediated acute/chronic organ rejection

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17
Q

T-cell functions

A

Type IV delayed cell-mediated hypersensitivity

CD4+ T cells= help B cell antibody production, make cytokines

  • IL-12–> Th1 cell
  • IL-4–> Th2 cell

CD8+ T-cells= Cytotoxic t-cells: kill VIRUS infected cells, neoplastic, donor graft cells. Secretes granules that contain:

  • perforin (deliver granules into target cell)
  • granzyme (serine protease= activates apoptosis in target cell)
  • Granulysin (antimicrobial, induces apoptosis)

Regulatory T-cell (Treg)

  • Express CD3, CD4, CD25 (alpha chain of IL-2 receptor)
  • Activated–> anti-inflammatory IL-10, TGF-beta
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18
Q

Dendrite cell

A

ONLY APC that can activate naive T-cell

  1. Phagocytoses foreign body
  2. Presented on MHC II–> Th (CD4+ cell) OR Presented on MHC I–> Cytotoxic (CD8+)
  3. Costimulation: B7 on dendrite–> CD28 on Naive T-cell
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19
Q

B cell activation/class switching

A

Th1 or Th2 (helper CD4+ T-cell) activated

  1. B-cell endocytosis foreign antigen
  2. Antigen presented on MHC II–> recognized by TCR on Th cell
  3. CD 40 on B-cell binds CD40Ligand on Th cell
  4. Th cell secretes cytokines–> Ig class switching of B cell
  5. B cell matures, produces antibodies
    • Mature B cells= IgM and IgD on surface
  • Differentiate into plasma cells secreting IgA, IgE, IgG

B-cell receptors:

  • Ig (duh)
  • CD19, CD20, CD21 (EBV receptor), CD40, MHC II, B7
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20
Q

Th1 cell

A

Helper T-cell

  1. Secretes IFN-gamma
  2. Activates macrophages
  3. Inhibited by IL-4, IL-10 (from Th2 cell)
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21
Q

Th2 cell

A

Helper T-cell

  1. Secretes IL-4, IL-5, IL-10, IL-13
  2. Recruits eosinophils for Parasite defense, promotes B-cell production of IgE
  3. Inihibited by IFN-gamma (from Th1 cell)
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22
Q

Antibody structure

A

Fab= Antigen binding fragment
- Only 1 antigenic specificity per B cell

Fc=

  • Constant
  • Carboxy terminal
  • Complement binding at CH2
  • Carbohydrate side chains
  • (Macrophage binds at CH3)

Diversity: Random, or somatic hypermutation after antigen stimulation

Role of Abs:

  • Opsonization
  • Neutralization: prevent bacterial adherence
  • Complement activation: enhanced opsonization
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23
Q

IgG

A 
Secondary response (delayed)
Most abundant

Roles:

  • Fixes complement
  • Crosses placenta
  • Opsonizes bacteria
  • Neutralizes toxins, viruses
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24
Q

IgA

A

Prevents bacterial/viral attachment to mucous membranes

Roles:

  • Does NOT fix complement
  • Does NOT cross placenta
  • Circulation= monomer
  • Secretion= dimer; crosses epithelial cells via trancystosis, picks up secretory component in epithelial cells
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25
Q

IgM

A

Primary response (immediate)

Roles:

  • Fixes complement
  • Does NOT cross placenta
  • Monomer (on B cell) or Pentamer
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26
Q

IgE

A

Type I hypersensitivity reaction

Roles:

  • Binds Mast cells/basophils
  • Cross-links when exposed to allergen
  • Releases histamine from mast cells
  • Activates eosinophil reaction to worms
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27
Q

Antigen type and memory (thymus dependent vs independent)

A

Independent: antigen LACKS peptide component

  • Cannot be presented by MHC (no peptide to present to T-cells)
  • Ex: LPS from gram-neg bacteria, polysaccharide capsule
  • NO immunologic memory

Dependent:

  • Antigens contain protein component
  • Ex: Diphtheria toxoid vaccine
  • Class switching and memory due to B-cell Th cell CD40-CD40L interaction
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28
Q

Complement pathway

A

Leads to formation of MAC (membrane attack complex) to defend against gram NEGATIVE bateria

Activation:

  1. Classic= IgG/IgM mediated
  2. Alternative= microbe surface molecules (attract C3b)
  3. Lectin= mannose/sugars on microbe

C3b= opsonization, clears immune complexes
C3a, C5a= anaphylaxis
C5a= neutrophil chemotaxis
C5b-C9= MAC formation–> cytolysis

** Pathway inhibited (from attacking self) by Decay-accelerating factor (DAF) and C1 esterase inhibitor

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29
Q

C1 esterase inhibitor deficiency

A

Hereditary angioedema

- ACE-I contraindicated

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30
Q

C3 deficiency

A

Recurrent pyogenic sinus, resp tract infections

- Increased susceptibility to Type-III hypersensitvity reactions (immune complex)

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31
Q

C5-C9 deficiencies

A

Recurrent Neisseria bacteremia

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32
Q

DAF deficiency

A

Complement-mediated lysis of RBCs

- Paroxysmal nocturnal hemoglobinuria

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33
Q

Macrophage cytokines

A

IL-1: fever, inflammation, recruit leukocytes
IL-6: fever, acute phase proteins
IL-8: Chemotactic factor for neutrophils
“Clean up on IL-8”: neutrophils clean up infection

IL-12: differentiate Th1–> activate NK cells
TNF-alpha: Septic shock, endothelial leak

34
Q

TH1 cell cytokines

A

IL-2: growth of helper, cytotoxic, Treg
IL-3: promotes bone marrow SC (GM-CSF)
IFN-gamma: activates macrophages, Th1, suppresses Th2; antiviral, antitumor

35
Q

Th2 cells cytokines

A

IL-2: growth of helper, cytotoxic, Treg
IL-3: promotes bone marrow SC (GM-CSF)
IL-4: differentiate Th2 cells, B-cell growth, class switching IgE, IgG
IL-5: Differentiate B cells, enhance IgA class switching, eosinophils
IL-10: inhibits actions of activated T cells and Th1

36
Q

Hot T-Bone stEAk

A 
IL-1: fever (hot)
IL-2: stimulates T cells
IL-3: stimulates Bone marrow
IL-4: stimulates IgE production
IL-5: stimulates IgA production
37
Q

Interferons

A

Place uninfected cells in antiviral state
“Interfere with viruses”: induce production of ribonuclease against viral mRNA

  • alpha, beta interferons= inhibit viral protein synthesis
  • gamma interferons= upregulate MHC I and MHC II expression, antigen presentation
  • activate NK cells to kill virus-infected cells
38
Q

Macrophage markers

A

CD14 (binds endotoxins/LPS from gram-negative bacteria)
CD40 (binds CD40L on helper T-cell)
MHC II + B7 (binds CD28 on T-cell)
Fc, C3b receptors (enhanced phagocytosis)

39
Q

NK cell markers

A

CD16: binds Fc of IgG
CD56: unique to NK cells**

40
Q

Live attenuated vaccine

A

Microorganism with capacity for growth and NO pathogenicity–> induces cellular response

Pro: life-long, strong immunity
Con: may revert to virulent form

Ex:
- Measles, mumps, rubella, polio (Sabin), varicella, yellow fever, Nasal flu (flumist)

41
Q

Inactivated (killed) vaccine

A

Pathogen inactivated by heat, chemicals
- Epitope structure of surface antigens maintained–> induces humoral immunity

Pro: stable, safer
Con: weaker immune response, need booster

Ex:
- Cholera, hep A, polio (salk), rabies

42
Q

Type I hypersensitivity reaction

A

Allergy (anaphylaxis, atopic):

  • rapid: free antigen cross-links IgE on mast cells/basohils
  • Test: skin test for specific IgE

Disorders:

  • Anaphylaxis
  • Allergic/atopic disorders
43
Q

Type II hypersensitivity reaction

A

Cytotoxic: IgM, IgG antibody mediated

  • Bind to antigen on foreign cell–> destruction via:
    1. Opsonization–> phaocytosis, complement
    2. Complement-mediated Lysis
    3. Antibody-dependent cell-mediated cytotoxicity (NK cells)

Test: direct, indirect Coomb’s

Disorders:

  • Autoimmune hemolytic anemia (AIHA)
  • Pernicious anemia
  • Idiopathic thrombocytopenic purpura
  • Erythroblastosis fetalis
  • Acute hemolytic transfusion reactions
  • Rheumatic fever
  • Goodpasture’s syndrome
  • Bullous pemphigoid (dermis, epidermis)
  • Pemphigus vulgaris (keratinocyte adhesion)
44
Q

Type III hypersensitivity reaction

A 
Immune-complex mediated
- Antigen-Antibody (IgG) complexes activate complement--> neutrophils attracted--> release lysosomal enzymes
Types:
- Serum sickness
- Arthus reaction

Disorders:

  • SLE
  • Polyarteritis nodosa
  • Post-strep glomerulonephritis
  • Serum sickness
  • Arthus reaction
45
Q

Serum sickness

A

Type III hypersensitivity reaction

  • Antibodies to foreign protein produced (after ~5 days)
  • Immune complex formation–> membrane deposition–> tissue damage

** Now mostly caused by drugs acting as haptens

46
Q

Arthus reaction

A

Type III hypersensitivity reaction

  • Intradermal injection of antigen–> antibodies fromation–> complex
  • Edema, necrosis, complement activation

Test: Immunofluorescent staining

47
Q

Type IV hypersensitivity reaction

A

Delayed (T-cell mediated) type:
- Sensitized T-cells encounter antigen–> release lymphokines–> macrophage activation

**4th, last
- Cell mediated (not transferrable in serum)
4 Ts: T-lymph, transplant rejections, TB skin test, Touching (contact dermatitis)

Test: patch test, PPD

Disorders:

  • MS
  • GBS
  • GVHD
  • PPD
  • Contact dermatitis
48
Q

Febrile nonhemolytic transfusion reaction (FNHTR)

A

Type II hypersensitivity reaction

  • Host antibodies against donor HLA antigens and leukocytes
  • Plasma spun to remove leukocytes

Symptoms:
- Fever, H/A, chills, flushing

49
Q

Acute hemolytic transfusion reaction (HTR)

A

Type II hypersensitivity reaction

  • ABO blood group incompatability–> intravascular hemolysis
  • Host antibody reaction against foreign antigen on donor RBCs–> extravascular hemolysis

Symptoms:
- Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinemia (intravascular), jaundice (extravascular)

50
Q

T-cell deficiency

A

Think AIDS
Bacterial sepsis

Viral infections: CMV, EBC, VZV, chronic infection with respiratory/GI viruses

Fungi/parasites: Candida, PCP

51
Q

B-cell deficiency

A

No antibodies, deficient complement-mediated processes
Bacteria: encapsulated (SHiN SKiS); recurrent bacterial infections

Viral: enteroviral encephalitis, poliovirus (live vaccine contraindicated)

Fungi/parasites: GI giardiasis (no IgA)

52
Q

Granulocyte deficiency

A

Staph aureus, burkholderia cepacia, serratia, nocardia

Fungi/parasites: candida, aspergillus

53
Q

Complement deficiency

A

Neisseria infections (no MAC)

54
Q

X-linked (Bruton’s) agammaglobulinemia

A

B-cell deficiency

Defect:

  • X-linked recessive
  • Defect in BTK (tyrosine kinase)
  • No B-cell maturation

Symptoms:
- Recurrent bacterial infections starting at 6 months

Finding:

  • Normal pro-B
  • Decreased B cells, maturation, Ig
55
Q

Selective IgA deficiency

A

B-cell deficiency

Defect: Unknown (most common primary immunodeficiency)

Symptoms:

  • Majority asymptomatic
  • Increased sinopulmonary infections
  • GI infections
  • Autoimmune disease
  • Anaphylaxis to IgA-containing blood products

Labs:

  • IgA < 7 mg/dL
  • Normal IgG, IgM, IgG
  • False positive beta-HCG due to heterophile antibody
56
Q

Common variable immunodeficiency (CVID)

A

B-cell deficiency

Defect in B-cell maturation

Symptoms:

  • 20s-30s,
  • Increased risk of autoimmune disease, lymphoma, sinopulmonary infections

Labs:

  • Normal B cell number
  • Decreased plasma, immunoglobulins
57
Q

Thymic aplasia (DiGeorge syndrome)

A

T-cell disorder

Defect: 22q11 deletion–> fail to develop 3rd, 4th pharyngeal pouches (thymus)

Symptoms:

  • Tetany (hypocalcemia due to no parathyroid glands)
  • Recurrent viral/fungal infections
  • Congenital heart, great vessel defects

Labs:
- No thymus, parathyroids–> decreased T cells, PTH, Ca+2

58
Q

IL-12 receptor deficiency

A

T-cell disorder

Defect: decreased Th1 response

Symptoms:
- Disseminated mycobacterial infections

Labs:
- Decreased IFN-gamma (secreted by Th1 cells–> suppresses Th2 cells; antiviral/antitumor)

59
Q

Hyper-IgE syndrome (Job’s syndrome)

A

T-cell disorder

Defect: Th1 cells fail to produce IFN-gamma–> neutrophils can’t respond to chemotactic stimuli

Presentation: FATED

  • coarse Faces
  • cold staph Abscesses
  • retained primary Teeth
  • increased IgE
  • Dermatologic problems (eczema)

Labs:
- Increased IgE

60
Q

Chronic mucocutaneous candidiasis

A

T-cell dysfunction

Symptoms:
- Candida infections of skin, mucous membranes

61
Q

Severe combined immunodeficiency (SCID)

A

B and T cell disorder

Defect:

  • Defective IL-2 receptor (most common, X-linked)
  • Adenosine deaminase deficiency

Presentation:

  • Failure to thrive
  • Chronic diarrhea
  • Thrush
  • recurrent viral, protazoal, bacterial, fungal infections
  • No thymus, germinal centers, B-cells

Labs:
- decreased T-cell recombination excision circles

Treatment:
- Bone marrow transplant (no allograft rejection)

** Vs Bruton’s= this has every type of infection (Bruton’s= bacterial), and B and T cells missing

62
Q

Ataxia-Telangiectasia

A

B and T cell defect

Defect:
- ATM gene= codes for DNA repair enzymes (can’t re-seal broken dsDNA- nonhomologous end-joining broken)

Symptoms:

  • Cerebellar defects (ataxia)
  • Spider angiomas (telangiectasia)
  • IgA deficiency

Labs:
- Increased alpha-fetoprotein

63
Q

Hyper-IgM syndrome

A

T and B cell defect

Defect:
- CD40L on helper T-cells defective: no class switching on B cells

Symptoms:
- Pyogenic infections early in life

Labs:

  • Increased IgM
  • Decreased IgG, IgA, IgE
64
Q

Wiskott-Aldrich Syndrome

A

B and T cell defect

Defect:

  • X-linked
  • WAS gene on X-chrom–> T-cells can’t reorganize actin cytoskeleton

Symptoms:

  • Thrombocytopenic purpura
  • Infections
  • Eczema

Labs:

  • Increased IgE, IgA
  • Decreased IgM
  • Thrombocytopenia
65
Q

Leukocyte adhesion deficiency

A

Genetic CD18 deficiency–> no integrin formation–> leukocytes can’t migrate from vasculature

Symptoms:

  • No pus formation
  • Late separation of umbilicus**
  • Poor wound healing

Labs:
- Neutrophilia

66
Q

Chediak-Higashi syndrome

A

Autosomal recessive:

  1. Lysosomal trafficking defect (LYST gene)
  2. Microtubule dysfunction in phagosome-lysosome fusion

Symptoms:

  • Recurrent pyogenic infections (staph and strep)
  • Albinisim
  • Peripheral neuropathy
  • nystagmus

Labs:
- Giant granules on neutrophils

67
Q

Chronic granulomatous disease

A

No NADPH oxidase
- No respiratory burst in neutrophils

Symptoms:

  • Susceptible to catalase-positive infections (can break down their own H2O2)= S. aureus, E. coli, aspergillus
  • WBCs can utilize H2O2 generated by invading organisms and convert to ROS (reactive oxygen species) if organism can’t degrade H2O2 (cat negative)

Labs:

  • Abnormal dihyrorhodamine (DHR) flow cytometry test)
  • Neutrophils don’t turn blue on nitro blue tetrazolium test

Tx: Gamma-interferon

68
Q

Acute transplant rejection

A

Weeks after transplant

Path:

  • Cell-mediated: cytotoxic T-lymphocytes react to foreign MHCs
  • Reversible with immunosuppression (cyclosporine, Muromonab-CD3)

Symptoms:
- Vasculitis of graft vessels, dense lymphocytic interstitial infiltrate

69
Q

Chronic transplant rejection

A

Months to years post-transplant

Path:

  • Class I MHC (non-self) seen by immune system as Class I MHC (self) presenting antigen–> destroy cell
  • Irreversible

Symptoms:

  • T-cell antibody-mediated vascular damage
  • Fibrosis of graft tissue, blood vessels
70
Q

Cyclosporine

A

MOA:

  • Binds cyclophilins
  • Inhibits calcineurin–> prevents IL-2 production–> blocks T-cells

Use: organ transplant, autoimmune disease

Tox:

  • Nephro, HTN, hyperlipidemia, hyperglycemia, tremor
  • Gingival hyperplasia, hirsutism
71
Q

Tacrolimus

A

MOA:

  • Binds FK-binding protein
  • Inhibits calcineurin–> prevents IL-2 production–> blocks T-cells

Use: Organ transplant

Tox:
- Nephro, HTN, hyperlipidemia, hyperglycemia, tremor

72
Q

Sirolimus

A

aka Rapamycin
MOA:
- Inhibits mTOR–> blocks IL-2 (T-cell proliferation)

Use: kidney transplant, drug-eluting stent

Tox:

  • Hyperlipidemia
  • Thrombocytopenia
  • Leukopenia
73
Q

Azathioprine

A

MOA:

  • Antimetabolite precursor of 6-mercaptopurine (interferes with pyramidine synthesis by blocking PRPP amidotransferase)
  • Toxic to lymphocyte proliferation

Use: kidney trans, autoimmune

Tox:

  • Bone marrow suppression
  • Metabolized by Xanthine Oxidase (XO)- beware with allopurinol administration
74
Q

Muromonab-CD3 (OKT3)

A

Monoclonal binding to CD3 on T-cells

Use: kidney trans

Tox:
- Cytokine release syndrome, Hypersensitivity reaction

75
Q

Filgrastim

A

G-CSF: granulocyte colony-stimulating factor

76
Q

Sargramostim

A

GM-CSF: granulocyte-macrophage colony-stimulating factor

- Like IL-3 from T-cells

77
Q

Alpha-IFN

A

Used for: Hep B, C, Kaposi’s, leukemia, malignant melanoma

78
Q

Beta-IFN

A

Used for MS

79
Q

Gamma-IFN

A

Used for Chronic Granulomatous disease Tx

80
Q

Infliximab, Adalimumab

A

TNF-alpha

  • Crohn’s, RA, psoriatic arthritis,
  • Ankylosing spondylitis (Infliximab)
81
Q

Herceptin (trastuzumab)

A

HER2-overexpressing breast cancer

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