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4. Immuno Flashcards

1
Q

This HLA type is associated with what disease? A3

A

hemochromatosis

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2
Q

This HLA type is associated with what disease? B27

A

Psoriatic Arthritis

Ank spondylitis

arthritis of Inflammatory Bowel Disease

Reactive arthritis

(PAIR) aka seronegative arthropathies

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3
Q

This HLA type is associated with what disease? DQ2/DQ8

A

Celiac

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4
Q

This HLA type is associated with what disease? DR2

A

Mult sclerosis, hay fever, SLE, Goodpasture

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5
Q

This HLA type is associated with what disease? DR3

A

Type I DM, SLE, Graves

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6
Q

This HLA type is associated with what disease? DR4

A

Rheumatoid arthritis, Type I DM

(4 walls in a “rheum”)

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7
Q

This HLA type is associated with what disease? DR5

A

Pernicious anemia –> B12 deficiency

Hashimoto’s thyroiditis

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8
Q

MHC I and II: present antigens to what cells?

A

Present antigen fragments to T cells and bind TCRs.

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9
Q

MHC I presents what kind of antigens to what cells?

A

Presents endogenously synthesized antigens (ie viral) to CD8+ cytotoxic T cells

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10
Q

MHC II presents what kind of antigens to what cells?

A

Presents exogenously synthized proteins (ie bacterial proteins and viral capsid proteins) to CD4+ T helper cells

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11
Q

NK cells: what do they do

A

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

(only lymphocyte member of the innate/acute immune system)

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12
Q

what enhances the activity of NK cells?

A

IL2, IL 12, IFN-beta, IFN-alpha

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13
Q

NK cells: what induces them to kill target cells?

A

induced to kill when exposed to a nonspecific activation signal on target cell

and/or to the absence of MHC I on a target cell surface

(all nucleated cells except RBCs express MHC I)

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14
Q

Major functions of B cells?

A
  • recognize antigen (via somatic hypermutation)
  • produce antibody (differentiate -> plasma cells to secrete immunoglobulins)
  • maintain immuno memory (memory B cells)
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15
Q

Major functions of T cells?

A
  • CD4+ T cells (HELPER) help B cells make antibody and produce cytokines
  • CD8+ T cells (KILLER) kill virus-infected cells directly
  • Delayed cell-mediated hypersensitivity (Type IV)
  • Acute and chronic cellular organ rejection
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16
Q

for the differentiation of T cells, where does the T cell precursor come from?

A

Bone marrow

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17
Q

what happens in the thymus in terms of differentiation of T cells?

A

T cells that are both CD4+ and CD8+ are separeted into CD4+ OR CD8+ cells

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18
Q

what is positive selection? where does it occur?

A

in the Thymic cortex

T cells that express TCRs capable of binding the surface self MHC molecules survive.

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19
Q

what is negative selection? where does it occur?

A

Thymic medulla

T cells expressing TCRs with high affinity for self antigens undergo apoptosis

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20
Q

what happens to CD4+ T cells in the lymph nodes?

A

differentiate into Th1 cells, Th2 cells, Th17 cells, and Treg cells (based on the influence of IL-12, IL-4, TGF-beta, and IL-6)

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21
Q

what does IL-12 do in the lymph node?

A

induces CD4+ T cells to differentiate into Th1 cells

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22
Q

what does IL-4 do in the lymph node?

A

influences CD4+ T cells to differentiate into Th2 cells

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23
Q

what does the combination of TGF-beta and IL-16 do in the lymph node?

A

induces CD4+ T cells to differentiate into Th17 cells

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24
Q

what does TGF-beta do in the lymph node?

A

induces CD4+ T cells to differentiate into Treg cells

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25
Q

what cells are antigen-presenting cells?

A

B cells, macrophages, dendritic cells

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26
Q

Process of activation for CD4+ T cell?

A
  • Foreign body phagocytosed by dendritic cell
  • Foreign antigen presented on MHC I and recognized by TCR on T helper cell. (signal 1)
  • Costimulatory signal is given by the interaction of B7 and C28 (signal 2)
  • Th cell activates and produces cytokines.
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27
Q

Process of activation for CD8+ T cell?

A
  • Foreign body phagocytosed by dendritic cell
  • Foreign antigen presented on MHC II and recognized by TCR on T killer cell. (signal 1)
  • Costimulatory signal is given by the interaction of B7 and C28 (signal 2)
  • Tc cell activates; recognizes & kills virus-infected cells
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28
Q

Process of B cell activation and class switching?

A
  • Helper T cell is activated
  • B cell endocytoses foreign antigen; presents it on MHC II. Recognized by TCR on Th cell. (signal 1)
  • B cell’s CD40 receptor binds the T cell’s CD40 ligand (signal 2)
  • Th cell secretes cytokines. –> determines Ig class switching of the B cell. B cell activates, undergoes class switching, affinity matulration and antibody production.
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29
Q

Th1 cells secrete what? activate what? inhibited by what?

A

Secrete IFN-gamma

Activate macrophages and cytotoxic T cells

Inhibited by IL4 and IL10 (from Th2 cell)

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30
Q

Th2 cells secrete what?

recruits what?

inhibited by what?

A

secrete IL-4, IL-5, IL-6, IL-13

Recruit eosinophils for parasite defense, and promote IgE production by B cells

Inhibited by IFN-gamma (from Th1 cell)

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31
Q

what is the overall interaction between macrophages and lymphocytes?

A

Macrophages release IL-12, which stimulates T cells to differentiate into Th1 cells.

Th1 cells release IFN-gamma to stimulate macrophages

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32
Q

what do cytotoxic T cells kill? generally, how do they do it?

A

Kill virus-infected, neoplastic, and donor graft cells

induce apoptosis

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33
Q

Cytotoxic T cells release cytotoxic granules containing what? what do the components of these granules do?

A

Cytotoxic granules contain preformed proteins:

  • Perforin: helps deliver content of granules into target cell
  • Granzyme B: serine protease; activates apoptosis inside target cell

Granulysin: antimicrobial; induces apoptosis

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34
Q

Lymph node: functions?

A

secondary lymph organ; functions are nonspecific filtration by macrophages, storage of B and T cells, immune response activation

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35
Q

what occurs in the Follicle of the lymph nodes?

A

B cell localization and proliferation.

located in outer cortex of node.

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36
Q

what are the 2 parts of the LN Medulla?

what does each part contain/do?

A

Medulla consists of medullary cords and medullary sinuses.

  • Medullary cords contain packed lymptocytes and plasma cells.
  • Medullary sinuses contain reticular cells and macrophages. Communicate with efferent (outgoing) lymphatics.
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37
Q

What does the Paracortex of LNs do? Where is it located?

Not well developed in what syndrome?

A
  • Houses T cells. Contains high endothelial venules through which T and B cells enter from blood (paracortex = pathway)
  • Located between follicles and medulla
  • Not well developed in patients with DiGeorge syndrome
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38
Q

during an extreme cellular immune response such as a viral infection, which part of the LN will enlarge?

A

Paracortex (contains endothelial venules for T and B cells to enter; houses T cells)

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39
Q

what structure drains lymph from the R side of the body above the diaphragm?

what does it drain into?

A

Right lymphatic duct.

Drains into junction of R internal jugular and R subclavian v

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40
Q

what structure drains lymph from everything except the R side of the body above the diaphragm?

what does it drain into?

A

Thoracic Duct.

Drains into Left Subclavian

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41
Q

what are the three main parts of a splenic sinusoid, and what is found at each place?

A
  1. Periarterial lymphatic sheath within white pulp: T cells
  2. Follicies within the white pulp: B cells (germinal centers)
  3. Marginal zone (btwn red pulp and white pulp): APCs and specialized B cells.
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42
Q

within a splenic sinusoid, where do APCs present their antigens?

A

in the marginal zone, between red pulp and white pulp

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43
Q

macrophages in the spleen remove what type of organisms?

A

encapsulated bacteria

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44
Q

2 reasons for splenic dysfunction?

how does splenic dysfunction lead to increased susceptability to encapsulated organisms?

A

splenectomy; sickle cell disease

Decreased IgM -> decreased complement activation -> decreased C3b opsonization -> increased susceptability to encapsulated organisms

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45
Q

what are the encapsulated bacteria that we worry about with asplenic patients?

A

SHiNE SKiS:

Strep pneumo

H influenza type B

Neisseria meningitidis (polysaccharide capsule: LOS)

E coli (K capsule)

Salmonella (Vi capsule)

Klebsiella (K capsule)

Group B Strep

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46
Q

what occurs in the Thymus?

from what embryonic structure does it derive?

A

T cell differentiation and maturation

From epithelium of 3rd pharyngeal pouches

(lymphocytes of mesenchymal origin)

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47
Q

Thymus: 2 parts? what cells are in each?

A
  • Cortex: dense, holds immature T cells
  • Medulla: pale, mature T cells & Hassall corpuscules containing epithelial reticular cells
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48
Q

T reg cells: what do they do?

what surface markers do they express? (4)

A
  • help maintain specific immune tolerance by suppressing CD4 and CD8 T cell functions
  • express cell surface markers CD3, CD4, CD25 (alpha chain of the IL-2 receptor), & tsn factor FOXP3
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49
Q

What do activated Treg cells do?

A

Produce anti-inflammatory cytokines (such as IL-10 and TGF-beta)

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50
Q

what parts of antibodies recognize antigens? heavy chain or light chain?

where is the antigen-binding site?

A

The variable parts of both Light and Heavy chains recognize antigens. (outermost portion of each chain)

antigen binding site is between the two chains on each side.

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51
Q

what portion of antibodies fixes complement?

A

The Fc portion. binds both complement and macrophages.

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52
Q

what part of an antibody determines its idiotype?

A

the Fab portion.

contains antigen-binding site, determines idiotype.

only one antigenic specificity expressed per B cell.

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53
Q

What are the 4 C’s of the Fc portion of an antibody? what is the 5th thing that the Fc portion does?

A
  • Constant region
  • Carboxy terminal
  • Complement binding
  • Carbohydrate side chains
  • Determines Isotype (IgM, IgD, etc)
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54
Q

How is antibody diversity generated? (4 ways)

A
  • random recombination of VJ (light chain) or VJ/VDJ (heavy chain) genes
  • random combination of heavy chains with light chains
  • somatic hypermutation following antigen stimulation
  • addition of nucleotides to DNA during recombination by terminal deoxynucleotidyl transferase
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55
Q

what are the 5 immunoglobulin isotypes

A

IgG, IgA, IgM, IgD, IgE

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56
Q

mature B lymphocytes express what on their surface?

how do we get cells that express the other immunoglobulin isotypes?

A

Express IgM and IgD.

they differentiate into plasma cells that secrete IgA, IgE, IgG in germinal centers (LNs) by isotype switching.

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57
Q

what mediates the isotype switching of mature B lymphocytes?

A

isotype switching = gene rearrangement

mediated by cytokines and CD40 ligand

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58
Q

IgG: functions?

A

main AB in the delayed response to an antigen.

fixes complement, crosses placenta (gives fetus passive immunity), opsonizes bacteria, neutralizes bacterial toxins and viruses.

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59
Q

IgA: functions?

A

prevents attachment of bacteria and viruses to mucus membranes. does not fix complement.

crosses epithelial cells by transcytosis. released into secretions (tears, saliva, mucus, early breast milk/colostrum).

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60
Q

IgA: what form is it present in in circulation? in secretions?

A

Circulation - Monomer

secretions - dimer

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61
Q

IgM: functions?

A

produced in the immediate response to an antigen. Fixes complement

does not cross placenta

antigen rceptor on the surface of B cells (along with IgD).

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62
Q

IgM: what forms is it present in?

A

on B cell: monomer

in secretions: pentamer. shape of pentamer allows it to trap free antigens out of tissue while humoral response evolves (remember IgM = part of immediate response to antigen)

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63
Q

IgD: function? located where?

A

unclear function

found on the surface of many B cells and in serum

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64
Q

IgE: function?

A
  • Binds mast cells and basophils; cross links when exposed to allergen
  • mediates Type I/immediate hypersensitivity reaction thru release of inflammatory mediators such as histamine.
  • Mediates immunity to worms by activating eosinophils.
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65
Q

which immunoglobin isotype is most abundant in serum? least?

A

most abundant: IgG

lowest concentration: IgE

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66
Q

what are thymus-independent antigens?

A
  • antigens lacking a peptide component. cannot be presented by MHC to T cells.
  • weakly- or non-immunogenic; vaccines often require boosters (ex pneumococcal polysaccharide vaccine)
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67
Q

what are thymus-dependent antigens?

A
  • antigen containing a protein component.
  • class switching and immunologic memory occur as a result of direct contact of B cells with Th cells (remember the CD40-CD40L interaction)
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68
Q

what are acute phase reactants? where are they produced? what induces them?

A
  • factors whose serum concentrations change significantly in response to inflammation
  • produced by the liver in both acute and chronic inflammatory states.
  • Induced by IL-6, IL-1, TNF-alpha, IFN-gamma
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69
Q

what acute phase reactants are upregulated in response to inflammation?

A

Serum amyloid A

CRP

Ferritin

Fibrinogen

Hepcidin

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70
Q

Each of these acute phase reactants is upregulated in response to inflammation: what does each do?

Serum amyloid A

CRP

Ferritin

Fibrinogen

Hepcidin

A

Serum amyloid A: function not given. (prolonged elevation can lead to amyloidosis)

CRP: Opsonin; fixes complement, facilitates phagocytosis. Measured clinically as a sign of inflammation.

Ferritin: Binds and sequesters iron to inhibit microbial iron scavenging

Fibrinogen: coagulation factor: promotes endothelial repair; correlates with ESR

Hepcidin: Prevents release of iron bound by ferritin -> anemia of chronic disease

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71
Q

what are the 2 acute phase reactants that are downregulated with inflammation? what does each do?

A
  • Albumin: reduction of albumin conserves amino acids for the reactants that are upregulated with inflammation
  • Transferrin: internalized by macrophages to sequester iron
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72
Q

Complement: what is a general overview?

A

system of interacting plasma proteins that play a role in innate immunity and inflammation.

MAC defends against gram-neg bacteria.

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73
Q

Complement system: three methods of activation?

A
  • Classic pathway: IgG or IgM mediated (GM makes Classic cars)
  • Alternative pathway: microbe surface molecules
  • Lectin pathway: mannose or other sugars on microbe surface

(See FA’14 p204 for extensive diagram)

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74
Q

Describe the functions of each of these parts of the complement cascade:

C3b

C3a, C4a, C5a

C5a

C5b-C9

A

C3b: Opsonization (C3b binds bacteria)

C3a, C4a, C5a: anaphylaxis (aaaa)

C5a: neutrophil chemotaxis

C5b-C9: cytolysis by Membrane Attack Complex (Big MAC attack)

75
Q

describe this complement disorder: C1 esterase inhibitor deficiency.

A

causes hereditary angioedema.

ACE inhibitors are contraindicated

(C1 is part of both the Lectin and Classic activation pathways)

76
Q

describe this complement disorder: C3 deficiency.

A

Increases risk of severe, recurrent pyogenic sinus and resp tract infections.

Increases susceptibility to Type III hypersens reactions.

77
Q

describe this complement disorder: C5-C9 deficiencies.

A

Increased susceptibility to recurrent Neisseria bacteremia

(recall C5-C9 –> MAC/membrane attack complex which causes cytolysis)

78
Q

describe this complement disorder: DAF (GPI anchored enzyme) deficiency.

A

Causes complement-mediated lysis of RBCs and paroxymal nocturnal hemoglobinuria

79
Q

Macrophages secrete 5 impt cytokines. what are they?

A

IL-1, IL-6, IL-8, IL-12, TNF-alpha

80
Q

briefly, what are the functions of IL-1 through IL-6?

(hints: generally they stimulate things. also there is an acronym)

A

HOT T-bone stEAK:

IL-1: Hot (fever)

IL-2: stimulates T cells

IL-3: stimulates bone marrow

IL-4: stimulates IgE production

IL-5: stimulates IgA production

IL-6: stimulates aKute-phase protein production

81
Q

IL-1: secreted by what cell? what is it also called? causes what?

what does it activate?

A

Secr by macrophages.

endogenous pyrogen; also called osteoclast-activating factor.

Causes fever & acute inflammation (the HOT in HOT T-bone stEAK)

activates endothelium to express adhesion molecules; induces chemokine secretion to recruit leukocytes

82
Q

IL-6: secreted by what cell? causes what?

A

Endogenous pyrogen (as is IL-1)

Secreted by both macrophages and Th2 cells

Causes fever and stimulates production of acute-phase proteins (aKute phase proteins… the K in “Hot Tbone stEAK”)

83
Q

IL-8: secreted by what cell? what does it do?

A

secreted by macrophages

major chemotactic factor for neutrophils

“Clean up on aisle 8” (neutrophils recruited by IL-8 to clear infections)

84
Q

IL-12: secreted by what cell?

what does it do?

A

secreted by macrophages and B cells

induces differentiation of T cells into Th1 cells

Activates NK cells

85
Q

TNF-alpha: what secretes it? what does it do?

A

secr by macrophages

mediates septic shock. activates endothelium. causes leukocyte recruitment, vascular leak.

86
Q

what two cytokines are secreted by ALL T cells?

A

IL-2 and IL-3

87
Q

IL-2: secreted by what? what does it do?

A

secr by all T cells

stimulates growth of helper, cytotoxic and regulatory T cells

88
Q

IL-3: secreted by what? what does it do?

A

secr by all T cells

supports growth and differentiation of bone marrow stem cells. functions like GM-CSF.

89
Q

Interferon-gamma: secreted by what? what does it do?

A

secreted by Th1 cells.

has antiviral and antitumor properties.

Activates NK cells to kill virus-infected cells; increases MHC expression and antigen presentation on all cells

90
Q

what 3 cytokines are secreted by Th2 cells?

A

IL-4, IL-5, IL-10

91
Q

IL-4: secreted by what? what does it do?

A

secr by Th2 cells

Induces differentiation into Th2 cells.

Promotes growth of B cells. Enhances class switching to IgE and IgG

92
Q

IL-5: secreted by what? what does it do?

A

secr by Th2 cells

promotes differentiation of B cells; enhances class switching to IgA.

Stimulates the growth and differentiation of eosinophils

93
Q

IL-10: secreted by what? what does it do?

A

secr by Th2 cells and Treg cells.

Modulates inflammatory response. Inhibits actions of activated T cells and Th1.

(similar to TGF-beta; both involved in inhibiting inflammation)

94
Q

what are interferons? (interferon alpha and beta)

A

part of innate host defense against both RNA and DNA viruses

(Interferons INTERFERE with viruses)

glycoproteins synthesized by viral-infected cells. act locally on uninfected cells, priming them for viral defense.

95
Q

what happens to cells that have been primed by interferon when they are infected with a virus?

A

viral dsRNA activates RNAaseL (degrades viral/host mRNA) and Protein kinase (inhibits viral/host protein synthesis).

Essentially results in apoptosis –> interrupts viral amplification in host.

96
Q

all T cells: what cell surface proteins do they have?

A

MHC I

TCR (binds antigen-MHC complex)

CD3 (assoc’d with TCR for signal transduction)

CD28 (binds B7 on APC)

97
Q

Th cells: what cell surface proteins do they have?

A

MHC I, CD4, CD40L

98
Q

Tc cells: what cell surface proteins do they have?

A

MHC I, CD8

99
Q

B cells: what cell surface proteins do they have?

A

MHC I

Ig (binds antigen)

CD19, CD20, CD21 (receptor for EBV), CD40

MHC II, B7

“Drink Beer at the Barr when you’re 21” – B cells/Epstein Barr virus/CD21

100
Q

Macrophages: what cell surface proteins do they have?

A

MHC I

CD14, CD40

MHC II, B7

Fc and C3b receptors (enhanced phagocytosis)

101
Q

NK cells: what cell surface proteins do they have?

A

MHC I

CD16 (binds Fc of IgG)

CD56 (unique marker for NK)

102
Q

define anergy.

what cells does it apply to?

A

the body fails to react to an antigen. applies to both T cells and B cells.

  • Self-reactive T cells become non-reactive without costim molecule
  • B cells also become anergic but tolerance is less complete than in T cells
103
Q

what are superantigens?

what bacteria have them?

A

bacterial toxins that can cross-link the beta region of the T cell receptor to the MHC II on APCs. Can thus activate any T cell –> massive release of cytokines!

S pyogenes and S aureus have superantigens.

104
Q

what are endotoxins/lipopolysaccharides? what bacteria have them?

A

bacterial toxins that directly stimulate macrophages by binding to endotoxin receptor CD14. Th cells not involved.

gram negative bacterian have them.

105
Q

what is antigenic variation?

give examples of Bacteria (3), Viruses (1), and Parasites (1)

A

mechanisms for variation of the organism. includes DNA rearrangement and RNA segment re-assortment

Bacteria: Salmonella (flagellar variants); Borrelia (relapsing fever); Neisseria gonorrhoeae (pilus protein)

Virus: influenza (minor variation = drift, major variation = shift)

Parasite: Trypanosomes (programmed re-arrangement)

106
Q

Passive immunity:

Means of acquisition?

onset?

duration?

examples?

A

Means of acquisition: receiving pre-formed antibodies

onset: rapid
duration: short span of antibodies (half-life = 3 weeks)
examples: IgA in breast milk, maternal IgG crossing placenta, antitoxin, humanized monoclonal ab.

107
Q

Passive immunity via delivery of preformed antibodies are given to patients with what exposures?

A

Tetanus toxin

Botulinum toxin

HBV

Rabies virus

“To Be Healed Rapidly!”

108
Q

Active immunity:

Means of acquisition?

onset?

duration?

examples?

A

Means of acquisition: exposure to foreign antigens

onset: slow
duration: long-lasting protection (memory)
examples: natural infection, vaccines, toxoid

109
Q

For Hep B or Rabies exposure, we can give Passive immunity via preformed antibodies; what else can we offer?

A

can also give combined passive and active immunizations for HBV or Rabies exposure. why not.

110
Q

Live attenuated vaccine: how does the vaccine work?

A

microorganism loses its pathogenicity, but retains capacity for transient growth within inoculated host.

Induces a cellular response.

111
Q

Live attenuated vaccine: Pros and cons?

A

Pros: induces strong, often lifelong immunity

Cons: may revert to virulent form. often contraindicated during pregnancy and for immunocompromised pts.

112
Q

Live attenuated vaccine: Examples?

A

Measles, Mumps, Rubella (MMR)

Polio (Sabin)

Influenza (intranasal)

Varicella

Yellow Fever

113
Q

Inactivated or killed vaccine: how does it work?

A

pathogen is inactivated by heat or chemicals; maintaining epitope structure on surface antigens is impt for immune response.

induces humoral immunity

114
Q

Inactivated or killed vaccine: Pros/cons?

A

Pros: stable, safer than live vaccines

Cons: weaker immune response. booster shots usually required.

115
Q

Inactivated or killed vaccine: examples?

A

Cholera

Hep A (series of shots)

Polio (Salk)

Influenza (injection; tell immunocompromised pts to get flu injection rather than intranasal)

Rabies (don’t want to give a live-attenuated vaccine for such a bad disease)

116
Q

Type I hypersensitivity reaction: describe the process.

what immune system components are involved?

A

Antibody-mediated reaction. IgE.

  • Anaphylactic and atopic - free antigen cross-links IgE on presensitized mast cells and basophils.
  • Triggers immediate release of vasoactive amines that act at postcapillary venules (ie histamine).
  • Reaction develops rapidly after antigen exposure due to preformed antibody.
  • Delayed response follows due to production of arachidonic acid metabolites (eg leukotrienes)
117
Q

Type II hypersensitivity reaction: describe the process.

what immune system components are involved?

A

Antibody mediated; cytotoxic (Cy-2-toxic). Antibody and complement lead to MAC.

IgM, IgG

IgM/IgG bind to antigen on enemy cell, leading to cellular destruction. Three mechs:

  • opsonization leading to phagocytosis or complement activation
  • complement-mediated lysis
  • antibody-dependent cell-mediated cytotoxicity, usually due to NK cells or macrophages.
118
Q

Test for Type II hypersens reaction?

A

Direct and Indirect Coombs’ test

Direct: detects antibodies that have already adhered to patient’s RBCs (test an Rh+ infant of an Rh- mom).

Indirect: detects antibodies that can adhere to other RBCs (test an Rh- woman for antibodies to Rh)

119
Q

Test for Type I hypersens reaction?

A

Skin test for specific IgE

120
Q

Type III hypersensitivity reaction: describe the process.

what immune system components are involved?

A

Immune complex reaction. (type III: 3 things stick together. antigen/antibody/complement)

Antigen-antibody complexes activate complement, which attracts neutrophils. Neutrophils release lysosomal enzymes.

121
Q

Serum sickness: describe. what type of hypersens reaction is it?

A

Type III/immune complex reaction

antibodies to foreign proteins are produced (5d). Immune complexes form, are deposited in membranes. There they fix complement -> tissue damage.

122
Q

Serum sickness: what causes it? what is presentation?

A

most serum sickness is caused by drugs acting as haptens (rather than serum).

Presentation: pt will have fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10d post exposure to an antigen.

123
Q

Arthus reaction: describe. what type of hypersens reaction?

how is it tested for?

A

local subacute antibody-mediated hypersensitivity Type III reaction.

intradermal injection of antigen induces antibodies, which form antigen-antibody complexes in the skin.

Characterized by edema, necrosis, complement activation.

Test via immunofluorescence staining.

124
Q

Type IV hypersensitivity reaction: describe the process.

what immune system components are involved?

A

Delayed, T cell mediated type. (therefore cannot be transferred by serum)

Sensitized T lymphocytes encounter antigen and release lymphokines

Leads to macrophage activation. no antibody involved.

125
Q

Type IV hypersens reaction: what are some examples when this reaction occurs?

How is it tested for?

A

the 4 Ts:

T lymphocytes

Transplant rejections

TB skin tests

Touching (ie contact dermatitis)

Test: patch test, PPD

126
Q

Very briefly, what is the main characteristic of each type of hypersensitivity reaction?

A

ACID:

Anaphlactic & Atopic (Type I)

Cytotoxic, antibody-mediated (Type II)

Immune complex (Type III)

Delayed, cell-mediated (Type IV)

127
Q

Type I hypersensitivity disorders: presentation?

2 examples?

A

immediate, anaphylactic, atopic

  1. Anaphylaxis due to bee sting, food/drug allergy
  2. Allergic and atopic disorders (rhinitis, hay fever, eczema, hives, asthma)
128
Q

Type II hypersensitivity disorders: presentation?

Examples (9)?

A

Presentation: specific to tissue or site where antigen is found.

  1. Autoimmune hemolytic anemia
  2. pernicious anemia
  3. idiopathic thrombocytopenic purpura
  4. erythroblastosis fetalis (Rh mediated hemolytic dz of newborn)
  5. Acute hemolytic transfusion reactions
  6. Rheumatic fever
  7. Goodpasture’s
  8. Bullous pemphigoid
  9. Pemphigus vulgaris
129
Q

Type III hypersensitivity disorders: presentation?

Examples (5)?

A

Presentation: vasculitis, systemic manifestations

  1. SLE
  2. Polyarteritis nodosa
  3. Poststrep glomerulonephritis
  4. Serum sickness
  5. Arthus reaction (swelling and inflammation following tetanus vaccine)
130
Q

Type IV hypersensitivity disorders: presentation?

Examples (5)?

A

Presentation: response is delayed, does not involve antibodies (Types I, II, III all involve antibodies)

  1. Multiple sclerosis
  2. Guillian-Barre
  3. Graft v Host disease
  4. PPD (test for TB)
  5. Contact dermatitis (eg poison ivy, nickel allergy)
131
Q

Allergic reaction to a blood transfusion: pathogenesis? clinical presentation? treatment?

A

Pathogenesis: Type I hypersens rxn against plasma proteins in transfused blood.

Presentation: urticaria, pruritis, wheezing, fever.

Tx: antihistamines

132
Q

Anaphylactic reaction to a blood transfusion: pathogenesis? clinical presentation?

A

Severe allergic reaction. IgA-deficient pts must receive blood products that lack IgA.

Presentation: dyspnea, bronchospasm, hypotension, resp arrest, shock

133
Q

Febrile nonhemolytic transfusion reaction: pathogenesis? clinical presentation?

A

Pathogenesis: Type II hypersens reaction. Host antibodies against donor HLA antigens and leukocytes.

Presentation: fever, headaches, chills, flushing

134
Q

Acute hemolytic transfusion reaction: pathogenesis? clinical presentation?

A

Type II hypersens reaction. Intravascular hemolysis (ABO blood type incompatibility)

or extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs)

Presentation: fever, hypotension, tachypnea, tachycardia, flank pain, hemoclobinemia (intravascular), jaundice (extravascular hemolysis)

135
Q

What is the disorder associated with this autoantibody: Anti-ACh receptor

A

Myasthenia gravis

136
Q

What is the disorder associated with this autoantibody: anti-basement membrane

A

Goodpasture

137
Q

What is the disorder associated with this autoantibody: anti-cardiolipin, lupus anticoagulant

A

SLE, antiphospholipid syndrome

138
Q

What is the disorder associated with this autoantibody: anticentromere

A

Limited scleroderma (CREST syndrome)

139
Q

What is the disorder associated with this autoantibody: anti-desmoglein

A

Pemphigus vulgaris

140
Q

What is the disorder associated with this autoantibody: anti-dsDNA, anti-Smith

A

SLE

141
Q

What is the disorder associated with this autoantibody: anti-glutamate decarboxylase

A

T1DM

142
Q

What is the disorder associated with this autoantibody: anti-hemidesmosime

A

Bullous pemphigoid

143
Q

What is the disorder associated with this autoantibody: anti-histone

A

drug-induced lupus

144
Q

What is the disorder associated with this autoantibody: anti-Jo-1, anti-SRP, anti-Mi-2

A

Polymyositis, dermatomyositis

145
Q

What is the disorder associated with this autoantibody: antimicrosomal, antithyroglobulin

A

Hashimoto thyroiditis

146
Q

What is the disorder associated with this autoantibody: antimitochondrial

A

1’ biliary cirrhosis

147
Q

What is the disorder associated with this autoantibody: antinuclear antibodies

A

SLE, nonspecific

148
Q

What is the disorder associated with this autoantibody: anti-Scl-70 (anti-DNA topoisomerase I)

A

Scleroderma (diffuse)

149
Q

What is the disorder associated with this autoantibody: anti smooth muscle

A

autoimmune hepatitis

150
Q

What is the disorder associated with this autoantibody: anti-SSA, anti-SSB (anti-Ro, anti-La)

A

Sjogren syndrome

151
Q

What is the disorder associated with this autoantibody: anti-TSH receptor

A

Graves disease

152
Q

What is the disorder associated with this autoantibody: anti-UI RNP (ribonucleoprotein)

A

Mixed connective tissue disease

153
Q

What is the disorder associated with this autoantibody: c-ANCA (PR3-ANCA)

A

Granulomatosis with polyangiitis (Wegeners)

154
Q

What is the disorder associated with this autoantibody: IgA antiendomysial, IgA anti-tissue transglutaminase

A

Celiac

155
Q

What is the disorder associated with this autoantibody: p-ANCA (MPO-ANCA)

A

Microscopic polyangiitis, Churg-Strauss syndrome

156
Q

What is the disorder associated with this autoantibody: Rheumatoid factor (antibody, most commonly IgM, specific to IgG Fc region), anti-CCP

A

Rheumatoid arthritis

157
Q

If a patient has no T cells, what problems will they have with Bacterial pathogens? Viral? Fungi/parasites?

A

Bacterial: sepsis

Viral: CMV, EBV, JCV, VZV, chronic infection with resp/GI viruses

Fungi/parasites: candida, PCP

158
Q

If a patient has no B cells, what problems will they have with Bacterial pathogens? Viral? Fungi/parasites?

A

Bacteria: Encapsulated (SHiNE SKiS)

Viral: Enteroviral encephalitis, poliovirus (live vaccine contraindicated)

Fungi/parasites: GI giardiasis (no IgA)

159
Q

If a patient has no granulocytes, what problems will they have with Bacterial pathogens? Viral? Fungi/parasites?

A

Bacteria: Staphylococcus, Burkholderia cepacia, Serratia, Nocardia

Viral: N/A

Fungi/Parasites: Candida, Aspergillus

160
Q

If a patient has no complement, what problems will they have with Bacterial pathogens? Viral? Fungi/parasites?

A

Bacteria: Neisseria (no MAC)

Viral: N/A

Fungi/parasites: N/A

161
Q

In general, B cell deficiencies produce what kinds of infections?

T cell deficiencies produce what kinds of infections?

A

B cell deficiencies: -> recurrent bacterial infections

T cell deficiencies: -> fungal/viral infections

162
Q

Defect in BTK (a tyrosine kinase gene) leads to what problem with immuno cells?

Name the disorder?

Presentation?

Lab/Exam findings?

A

Defect in BTK -> no B cell maturation. X linked recessive.

Disorder: X-linked (Bruton) agammaglobulinemia

Presentation: Recurrent bacterial and enteroviral infections after 6 mo (covered by maternal IgG until then)

Findings: Normal CD19+ B cell count, decreased pro-B, decreased Ig (all classes).

Exam: absent/small lymph nodes and tonsils

163
Q

Most common primary immunodeficiency (B cell disorder) - name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: Selective IgA deficiency (specific defect is unknown)

Presentation: majorly Asymptomatic. may be airway and GI infections, autoimmune disease, atopy, anaphylaxis to IgA-containing products

Findings: IgA < 7 mg/dL with normal IgG and IgM levels

164
Q

Defect in B cell differentiation (from many causes) - name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: common variable immunodeficiency

Presentation: acquired in 20s-30s. incr risk of autoimmune disease, bronchiectasis, lymphoma, sinopulm infections

Findings: decr plasma cells, decr immunoglobulins.

165
Q

22q11 deletion; failure to develop 3rd/4th pharyngeal pouches - name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: Thymic aplasia (DiGeorge syndrome). absence of thymus and parathyroids

Presentation: Tetany (due to hypocalcemia), recurrent viral/fungal infections (T cell deficiency), conotruncal abnormalities (tetralogy of Fallot, truncus arteriosus)

Findings: decr T cells, decr PTH, decr Ca2+. 22q11 deletion detected by FISH

166
Q

Autosomal recessive, decreased Th1 response - name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: IL-12 receptor deficiency.

Presentation: disseminated mycobacterial and fungal infections; may present after BCG vaccine

Findings: decr IFN-gamma

167
Q

deficiency of Th17 cells due to STAT3 mutation -> decr recruitment of neutrophils to sites of infection - name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: Autosominal dominant hyper-IgE syndrome (Job syndrome)

Presentation: FATED - coarse Facies, cold (not inflammed) staph Abscesses, retained primary Teeth, incr IgE, Dermatologic problems (eczema)

Findings: incr IgE; decr IFN-gamma

168
Q

T cell dysfunction due to many causes - name a possible disorder?

Presentation?

Lab/Exam findings?

A

Disorder: Chronic mucocutaneous candidiasis

Presentation: noninvasive Candida infection of skin and mucous membranes

Findings: absent in vitro T cell prolif in response to Candida antigens, absent cutaneous reaction to Candida antigens

169
Q

defective IL-2R gamma chain or adenosine deaminase deficiency - name the disorder?

Presentation?

Treatment?

Lab/Exam findings?

A

Disorder: Severe Combined Immunodeficiency (SCID) - deficiency in both B cells and T cells

Presentation: Failure to thrive, chronic diarrhea, thrush, recurrent viral,bacterial, fungal, protozoal infections

Treatment: bone marrow transplant (note no concern for rejection)

Findings: decr T cell receptor excision circles (TRECs), absence of thymic shadow on CXR, absence of germinal centers on LN biopsy, absence of T cells on flow cytometry

170
Q

Defects in ATM gene -> DNA double strand breaks -> cell cycle arrest - name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: Ataxia-telangiectasia (ATM = Ataxia-Telangiectasia Mutated). Bottom line: IgA deficiency causes defect in DNA repair enzymes

Presentation: Triad: cerebellar defects (Ataxia), spider Angiomas (telangiectasia), IgA deficiency

Findings: Incr AFP, decr IgA, decr IgG, decr IgE

Lymphopenia, cerebellar atrophy

171
Q

defective CD40L on Th cells - name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: Hyper-IgM syndrome (class switching defect)

Presentation: severe pyogenic infections early in life; opportunistic infections with Pneumocystis, Cryptosporidium, CMV

Findings: Incr IgM, decr IgG/IgA/IgE

172
Q

Mutation in WAS gene -> T cells unable to recognize actin cytoskeleton - name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: Wiskott-Aldrich syndrome

Presentation: WATER: Wistott-Aldrich: Thrombocytopenic purpura, Eczema, Recurrent infections

Incr risk of autoimmune dz and malignancy

Findings: decr/nl IgG/IgM. Incr IgE, IgA. fewer/smaller platelets

173
Q

defect in LFA-1 integrin (CD18) protein on phagocytes - name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: Leukocyte adhesion deficiency (Type 1). Impaired migration and chemotaxis.

Presentation: recurrent bacterial skin and mucosal infections, absent pus formation, impaired wound healing, delayed separation of umbilical cord (>30d)

Findings: incr neutrophils. Neutrophils not present at infection sites.

174
Q

defective lysosomal trafficking regulator gene (LYST) - name the disorder?

Presentation?

Lab/Exam findings?

A
175
Q

Chediak-Higashi syndrome (microtubule dysfunction in phagosome-lysosome fusion)

Presentation: Recurrent pyogenic infections by staph and strep; partial albinsm; peripheral neuropathy; progressive neurodegeneration; infoltrative lymphohistiocytosis

Findings: giang granules in neutrophils and platelets; pancytopenia; mild coag defects

A
176
Q

Defect of NADPH oxidase causing decr reactive oxygen species and absent resp burst in neutrophils- name the disorder?

Presentation?

Lab/Exam findings?

A

Disorder: chronic granulomatous disease

Presentation: incr susc to catalase + organisms (PLACESS: Pseudomonas, Listeria, Aspergillus, Candida, E coli, S aureus, Serratia)

Findings: abnormal dihydrorhodamine test (flow cytometry); nitroblue tetrazolium dye reduction test is -.

177
Q

Autograft: origin of tissue is ?

A

From self

178
Q

Syngeneic graft: origin of tissue is ?

A

from identical twin or clone

179
Q

Allograft: origin of tissue is ?

A

from nonidentical individual of same species (sib, stranger)

180
Q

Xenograft: origin of tissue is ?

A

from different species

181
Q

Transplant rejection within minutes is what type?

Pathogenesis? features?

A

Hyperacute

Pre-existing recipient antibodies react to donor antigen (Type II reaction) & activate complement

Features: widespread thrombosis of graft vessels -> ischemia/necrosis. Graft must be removed.

182
Q

Transplant rejection within weeks to months is what type?

Pathogenesis? features?

A

Acute

Cellular pathogenesis: CTLs activated against donor MHCs.

Humoral pathogenesis: sim to hyperacute rejection, except antibodies develop after transplant (not pre-formed)

Features: vasculitis of graft vessels with dense interstitial lymphocytic infiltrate.

Prevent/reverse with immunosuppressants.

183
Q

Transplant rejection within months to years is what type?

Pathogenesis? features?

A

Chronic

Pathogenesis: Recipient T cells perceive donor MHC as recipient MHC, and react against donor antigens presented. Both humoral and cellular components.

Features: Irreversible. T cell and antibody-mediated damage.

Organ specific: Heart –> atherosclerosis. Lungs –> bronchiolitis obliterans. Liver –> vanishing bile ducts. Kidney –> vascular fibrosis, glomerulopathy

184
Q

Graft v Host disease: speed of onset?

Pathogenesis?

Features?

A

Onset: variable

Pathogenesis: Grafted immunocompetent T cells proliferate in immunocompromised host and reject host cells with “foreign” proteins -> severe organ dysfunction.

Features: maculopapular rash, jaundice, diarrhea, HSM.

Usually in bone marrow and liver transplants (rich in lymphocytes).

**Potentially beneficial in bone marrow transplant for leukemia (graft v tumor effect)

x First Aid (17 decks)

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