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Immuno Flashcards

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1
Q

Lymph node structure

Where are...
B-cells?
T-cells?
Lymphos/plasma cells?
Macs/retics?
A

fxn: nonspecific filtration by macs, lympho storage

follicle - B-cells! primary (outer) = dense/dormant. secondary (inner) = germinal centers, active

medulla - medullary cords (lymphos + plasma cells), sinuses (reticular cells, macs)

paracortex - houses T cells, T/B cells enter from blood, site of engorgement during immune response

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2
Q

Spleen sinusoids

Where are…
T cells?
B cells?
APCs?

A

Red pulp = mechanical filtration of RBCs by fenestrated BM and macs, led to trabeculae

White pulp =
- periarteriolar lymphatic sheath (PALS): T cells
- follicles: B cells
Marginal zone = APCs capture blood-borne antigens for recognition by lymphocytes

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3
Q

Post-splenectomy findings

A

Howell-Jolly bodies (nuclear remnants in an RBC)

Target cells

Thrombocytosis

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4
Q

Thymus structure

Where are…
immature T cells?
mature T cells?

Where do positive and negative selection occur?

A

T-cell differentiation and maturation
derived from Third pharyngeal pouch
Cortex = immature T cells (site of positive selection: only T cells expressing TCRs that bind self-MHC survive)
Medulla = pale, mature T cells (site of negative selection: T cells with TCRs for high-affinity self-antigen binding are apoptosed)

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5
Q

innate vs. adaptive immunity

A

innate - secreted proteins: lysozyme/complement/CRP, TLRs recognize PAMPs (LPS, flagellin, ssRNA)

adaptive - variation through VDJ recomb, based on Igs

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6
Q

MHC I

A
  • MHC I: HLA-A, HLA-B, HLA-C, all nucleated cells
  • present viral/cytosolic proteins to CD8 cells
  • loading happens in RER
  • assoc with B-microglobulin
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7
Q

MHC II

A
  • MHC II: HLA-DR, HLA-DP, HLA-DQ,
  • binds CD4,
  • expressed on APCs only,
  • loading happens in acidified endosome with invariant chain
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8
Q

HLA subtypes and disease

A

A3 - hemochromatosis
B27 - PAIR: psoriatic arthritis, ank spondy, IBS, reactive arthritis
DQ2/DQ8 - celiac disease
DR2 - multiple sclerosis, hay fever, SLE, Goodpasture
DR3 - DM Type I, SLE, Graves, Hashimoto
DR4 - DM Type I, Rheum (4 walls in a room)
DR5 - pernicious anemia

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9
Q

NK cells function, cytokines, signals for activation

A 
Apoptosis induction (using perforin and granzymes)
Enhanced by IL-2, IL-12, IFN-a, IFN-B
2 signals: non-specific activation signal, absence of class I MHC
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10
Q

Helper T cells (CD4+)

Th1 (phagocytosis/cell-mediated) vs. Th2 (antibody response)

Give activating and inhibiting cytokines

A

Th1 = secretes IFN-y, macs/cytotoxic T, activated by IFN-y and IL-12 (from macs), inhibited by IL-4/10 (from Th2)

Th2 = secretes IL-4/5/10/13, activate B cells and recruit eosinophils, activated by IL-4, inhibited by IFN-y (from Th1)

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11
Q

Cytotoxic T cells function

A

Release cytotoxic granules containing preformed proteins (perforin, granzyme) to induce apoptosis

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12
Q

Regulatory T cells

A

Maintain specific immune tolerance by suppressing CD4/CD8 T cells

Look for: CD3/4/25, FoxP3

Produce IL-10, TGF-B

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13
Q

Naive T-cell activation

A
  1. DC samples/processes antigen
  2. DC migrates to draining lymph node
  3. MHC II/I presents foreign antigen to CD4/8
  4. Costimulatory signal is given by interaction of B7 and CD28 (if no second signal, then anergy)
  5. Th cell activates and produces cytokines. Tc cell activates and destroys
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14
Q

B-cell activation

A
  1. Th cell activation
  2. B-cell receptor mediated endocytosis, foreign antigen is presented to helper T
  3. CD40 receptor on B cell binds CD40L on helper T cell
  4. Helper T secretes cytokines to stimulate Ig class switching of B cell (IL-4, IL-5)
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15
Q

Antibody structure, function, diversity (3 mechs)

A

Light and heavy chains (light = Fab only, heavy = both),

Fc binds complement (one arm, Constant, Carboxy terminal, Complement, Carbo side chains)
Fab binds antigen (two arms)

Diversity: VJ/VDJ recomb, somatic hypermutation, terminal deoxynucleotidyl transferase (DNA nuc addition)

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16
Q

IgG, IgA, IgM, IgE

A

IgG - fixes complement, crosses placenta
IgA - prevents microbe attachment to mucous membranes, does not fix complement, produced in GI tract to protect against GI infxns, released in secretions as a dimer (notably breast milk)
IgM - immediate response to antigen, serves as antigen receptor to B cells, pentamer form allows avid binding to antigen
IgE - binds mast cells/basophils, cross-links when exposed to allergen, mediates Type I hypersensi rxn, mediates worm resistance through Eos

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17
Q

Acute phase reactants (produce in liver in response to inflammation, induced by IL-6)

A

Upregulated: CRP (fixes complement), ferritin (sequesters iron), fibrinogen (coagulation factor, correlates with ESR), hepcidin (prevents release of iron bound to ferritin, leads to AOCD)

Downregulated: albumin (reduction conserves amino acids for acute phase proteins), transferrin (sequester iron)

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18
Q

Complement pathways

A

Classic - IgG, IgM mediated (GM makes classic cars), C1
Alternative - microbe surface molecules, C3
Lectin - mannose or other sugars on microbe surface, C1-like complex

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19
Q

Complement proteins (3b, 3a/4a/5a, 5b-9, DAF)

A

C3b - opsonization, C3b binds bacteria (also helps clear immune complexes)
C3a/4a/5a - anaphylaxis (5a also does neut chemotaxis)
C5b-9 - cytolysis by MAC

Inhibitors: DAF = CD55, combines with C1 esterase inhibitor to help prevent complement activation on self cells

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20
Q

Complement disorders

A

C1 esterase inhibitor deficiency (results in longer C1 half life) - hereditary angioedema, ACEis are contraindicated
C3 deficiency - increases severe, recurrent sinopulmonary infections, increased Type III hypersensitvity rxns (lack of immune complex clearance)
C5-C9 deficiencies - increased Neisseria infections
DAF deficiency - complement-mediated destruction of RBCs (hemolysis). PNH (dz of decreased GPI-anchored proteins) leads to DAF (GPI-anchored protein) deficiency

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21
Q

Important cytokines secreted by…

Macrophages
All T cells
Th1 cells
Th2 cells

Study These Flashcards
A

Macrophages:
Hot T-Bone stEAK: 1 = fever, 2 = stimulate T cells, 3 = bone marrow (GM-CSF analog), 4= IgE, 5= IgA, 6= aKute phase reactants
IL-8: chemotaxis for neutrophils
IL-12: differentiation of T cells into Th1 cells, NK activator
TNF-a: septic shock, WBC recruitment, vascular leak

Th1 cells:
IFN-y: stimulates macs to kill pathogens (also activates NK cells to kill virus-infected cells)

Th2 cells:
Il-10: modulates inflammatory response, decreases cytokines, inhibits macs/DCs (works in concert with TGF-b)

22
Q

Respiratory burst, NADPH oxidase, CGD

Study These Flashcards
A

Activation of neutrophil NADPH oxidase, leads to rapid release of ROS/hypochlorite to kill microbes

CGD: phagocytes don’t make their own peroxide (due to lack of NADPH oxidase) so use microbial peroxide. However, microbes with their own catalase (which breaks down peroxide) survive! Watch for S. aureus and Aspergillus

23
Q

Interferons

Study These Flashcards
A

Glycoproteins synthesized by virus-infected cells that act locally on non-infected cells to ramp up viral defenses.

Essentially results in apoptosis.

“Interfere with viruses”

24
Q

Superantigens

Endotoxins

Study These Flashcards
A 
Superantigen: cross-link B-region of T-cell receptor to the MHC class II on APCs
- T cells (IL-2) and macrophages (IL-1 and TNF-a) lead to massive cytokine release

Endotoxin: direct stimulation of macrophages by binding to endotoxin receptor TLR4

25
Antigenic variation
bacteria: Salmonella (flagella), Borrelia recurrentis (relapsing fever), N. gonorrheae (pilus) viruses: influenza, HIV, HCV parasites: trypanosomes
26
Administration of preformed antibodies
Passive immunity Rapid onset Tetanus, Botulinum, HBV, Varicella, Robies ex: breast milk (IgA dimers), placental (IgG), antitoxin
27
Exposure to foreign antigens
Active immunity | slow onset, long-lasting protection
28
Vaccine with cellular and humoral responses
Live, attentuated vaccine Microbe has lost pathogenicity but retains capacity for growth Life long immunity MMR, polio (sabin), intranasal flu, chicken pox, yellow fever
29
Vaccine with only humoral response
Inactivated/Killed vaccine Epitope structure is maintained on surface antigens Weaker immune response, booster shots required RIP Always: Rabies, Influenza (shot), Polio (Salk), hep A
30
Anaphylactic hypersensitivity
Type I free antigen cross-links IgE, triggers mast cell and basophil degranulation (delayed response = leukotrienes) First and Fast test: skin test for specific IgE
31
Cytotoxic hypersensitivity
Type II - cy-two-toxic IgM/IgG bind antigen on foreign cell, tag for destruction (phagocytosis, complement-mediated inflammation, Ab-mediated cellular dysfunction) Direct Coombs': detect antibodies that have adhered to RBCs Indirect Coombs': detect free serum antibodies that can adhere to RBCs
32
Immune complex mediated hypersensitivity
Type III (3 things! Antigen - antibody - complement) Immune complex attract neutrophils, which release lysosomal enzymes serum sickness - 5 days post-exposure, deposition of complexes in membranes leading to tissue damage. Now commonly caused by drugs, look for fever, urticaria, arthralgia, etc. Arthus reaction - local subacute rxn after intradermal injection of antigen. Look for edema, necrosis, activation of complement
33
T-cell mediated hypersensitivity
Type IV - delayed 4 T's: T cells, Transplant rejection, TB skin test, Touching Sensitized T cells release cytokines after stimulation by antigen. No antibodies involved!
34
``` Examples of disorders Type I Type II Type III Type IV ```
I: Allergic/atopic disorders, anaphylaxis II: antibody mediated hemolysis, Goodpasture, Graves, GB syndrome, ITP, MG, rheumatic fever III: Arthus rxn, SLE, polyarteritis nodosa, PSGN (vasculitidies) IV: Contact derm, GVHD, MS, PPD (no antibodies!)
35
Blood transfusion reactions
Allergic - Type I against plasma proteins Anaphylaxis - severe allergic rxn (breathing problems) Febrile non-hemolytic - Type II, host antibodies against donor HLA antigens and WBCs Acute hemolytic - Type II, intravascular/ABO incompatibility (hemoglobinuria) or extravascular/host antibody rxn (jaundice)
36
Recurrent bacterial/enterovial infections after age of 6mos (loss of maternal IgG)
X-linked agammaglobulinemia B's! Defect in BTK, no B-cell maturation, X-linked recessive (more common in Boys) Look for absent B cells in peripheral blood and low number of all immunoglobulins
37
Airway/Gi infections, Autoimmune disease, Atopy
Selective IgA deficiency Asymptomatic. Airway/Gi infections, Autoimmune disease, Atopy, Anaphylaxis to IgA-containing products
38
Autoimmune disease, brochiectasis, lymphoma, sinopulmonary infections
Common variable immunodeficiency Defect in B-cell differentiation. Can be acquired in 20s-30s. Decreased plasma cells and decreased immunoglobulins
39
Tetany, recurrent viral/fungal infections, conotruncal abnormalities
``` Thmyic aplasia (DiGeorge) - 22q11 deletion failure to develop 3rd and 4th branchial pouches (absent thymus and parathyroid), T cell disorder ``` Decreased T cells, PTH, Ca2+
40
Disseminated mycobacterial and fungal infections; appears after BCG vaccine (decreased Th1 response)
IL-12 deficiency Decreased Th1 response. Autosomal recessive. Decreased IFN-y
41
coarse Facies, Abscesses, Teeth, increased igE, Derm lesions (FATED)
autosomal dominant hyper-IgE syndrome (Jobs) | deficiency of Th17 cells due to STAT3 defect --> impaired neutrophil recruitment to site of infection
42
Noninvasive Candidal infections
Chronic mucocutaneous candidiasis T-cell dysfunction, absent T cell proliferation to Candidal antigens
43
Failure to thrive, chronic diarrhea, thrush. Recurrent bacterial, viral, fungal infections
Severe combined immunodeficiency (SCID) Major types: IL-2R deficiency, adenosine deaminase deficiency tx: bone marrow transplant (no concern for rejection)
44
Cerebellar defects, spider angiomas/telengiectasias, IgA deficiency
Ataxia-telengiectasia Defects in ATM gene --> failure to repair DNA double stand breaks --> cell cycle arrest increased AFP, decreased IgA/G/E, lymphopenia Also, hypersensitivity to ionizing radiation
45
Severe pyogenic infections, opportunistic infections, only IgM present
Hyper-IgM syndrome | Defective CD40L on T cell leads to inability for B cells to undergo class-switching
46
Thrombocytopenic purpura, eczema, recurrent infections
Wiskott-Aldrich (WATER) Mutation in WAS gene = T cells unable to reorganize actin cytoskeleton Increased risk of autoimmune disease and malignancy low to normal IgG, IgM, increased IgE, IgA Fewer and smaller platelets
47
Recurrent skin/mucosal infections, absent pus, impaired wound healing, delayed separation of umbilical cord
Leukocyte Adhesion Deficiency type 1 Defect in LFA-1 integrin (CD18) on phagocytes --> impaired migration and chemotaxis Increased neutrophils, but absence at infection sites
48
Recurrent staph/strep infections, partial albinism, peripheral neuropathy, neurodegeneration
Chediak-Higashi Defect in lysosomal trafficking regular gene (LYST) Microtubule dysfunction in phagosome-lysosome fusion Look for giant granules in granulocytes and platelets
49
Increased susceptibility to catalase + organisms (Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E. coli, S. aureus, Serratia)
Chronic granulomatous disease Defect of NADPH oxidase --> decreased ROS/respiratory burst in neutrophils Abnormal dihydrorhodamine test
50
Transplant rejections minutes... weeks to months... months to years...
Hyperacute - pre-exisiting antibodies in recipient react to donor antigen (type II hypersensivity) - leads to widespread thrombosis/ischemia/necrosis Acute - CD8 T cells activate against donor MHCs and antibodies develop after transplant. Vasculitis with dense interstitial lymphocytic infiltrate. Prevent with immunosuppressives! Chronic - CD4 T cells respond to recipient APCs presenting donor peptides, secrete cytokines, leads to proliferation of vascular smooth muscle and parenchymal fibrosis
51
Graft-vs-host disease
Grafted T cells proliferate in the recipient due to immunocompromised status (usually after liver/BMT) Also, rash, jaundice, diarrhea, HSM Potentially beneficial after BMT for leukemia
52
Immunosuppresants
IL-2 transcription blockers - cyclosporine (cyclophilin), tacrolimus (FKBP), both are very nephrotoxic IL-2 response blocker - sirolimus (binds mTOR), not nephrotoxic, good for kidney transplant Nucleotide synth blocker - azathioprine (6-MP precursor), good for other AI dzs, toxicity increased by allopurinol (6-MP degraded by xanthine oxidase) Steroids - NF-KB inhibitor, suppress cytokine transcription, iatrogenic Cushing syndrome

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