Immunology Stuff

Question 1

• Immune problem from hematopoiteic stem cell to lymphoid stem cell? Low what? Survivorship?
• Problem after pre B cells? Genetics? Normal what? Leads to?
• Problem class switching? Which switch? Genetics? Defective what?
• Difficult to trigger Ab?
• No t cells? Chrom? Also effected?
• Pure B cell deficiency leads to?
• Pure T cell deficiency leads to?
• Clinical features of DiGeorge? (5)
• IgA deficiency: Most common? Percent? Symptoms?
• Nude mouse model: Fail to make what? Similar?

Answer 1

• SCID; B and T; low
• Burtons; X linked; T cells; agammaglobinemia
• Hyper IgM; IgM –> IgG; x linked; IgM
• Common variable
• DiGeorge; 22; parathyroid
• High grade pus producing pathogens
• Increased viruses, yeasts, fungi
• CATCH; cardiac issues, abnormal facies, thymic aplasia, cleft palate, hypocalcemia and hypothyroidism
• Immunodeficiency, 1/500; asymptomatic or allergies/sinopulmonary infections
• Fail to make thymic stroma; DiGeorge

Question 2

• SCID: 1.) Genetics? Receptor mutation?
  2.) Genetics? Enzyme defic.? Leads to? Treatment options? Problem with retrovirus vectors?
  Transplant: For Digeorge? SCID? Success? Can also do?
• Gamma globin IVIG: Used when? What is in the infusion? Half life? Problem with this? (2) New possible treatment?
• B Cell tests? (2)
• T Cell tests? (2)
• Phago tests? (2)
• Complement test? (2)
• Immunosupresive viruses? (4)

Answer 2

• X linked recessive; IL-2
• AR; Adenosine deaminase; Incr. adenosine; Pure ADA drug; vectors are tough to control
• Fetal thymus; Bone Marrow; 50% GvH; purified stem cells
• B Cell deficient; 99% IgG; 3 weeks; short supply and expensive; SCIG for home use
• Sequenceing, serum protein electro.
• Skin test, marker counts
• Oxidative burst, chemotaxis assay
• CH50 and C1 inh. assay
• Measles, mononucleolis, CMV, AIDS

Question 3

• Chronic frustrated immune response:
• TGFbeta favors? which is abundant where? Leads to? DC’s make what? Favors? What else are common? Why?
• TGFbeta + IL6: Favors what? Down regulate what? IL6 produced where? In response to?
• Chronic immune diseases likely related to?
• IBD: Dysfunctional immune response against what? What else has been found? Shared between both? What allows defensens back in? What else plays a role?

Answer 3

• Treg cells; peyers patches; TH0 to Treg differ.; IL10; Tregs; Tfh cells driving B cells to IgA; mucus
• TH1/TH17; Treg; gut epithelia; stress
• Insufficient Treg regulation
• commensal bacteria; many LOCI often mutated; NOD2 gene; leacky epithelia; bad luck

Question 4

• Chronic frustrated immune response:
• Celiac disease:Enteropathy of what? Can lead to what? (3) Transglutamase cross links and can’t release what? Turns it into? Where is this a problem? Genetic component with HLA? But? Skin?
• What happens with Be exposure? What binds it?
• Hygeine hypothesis: What may help immune system?
• Old friends hypothesis: Harmless organisms do what? Leads to increased what?
• Whipworm study thought that? What actually happened when given to Crohns patients?

Answer 4

• gluten; malabsorption, diarrhea, failure to thrive; gluten; auto-antigen; endomysium; 90% HLA-DQ2; 10% HLA-DQ8; many have this and don’t get celiac disease; IgA attack similar strain
• Macs eat it and can’t digest it; glutamic acid
• Dirt and exposore to pathogens
• harmless organisms help instruct immune system; Treg
• Parasites would increase TH2; Increased Treg and supressed TH1/TH2/TH17

Question 5

• Type 2 immunopathy:
• Due to actions of? Targeting?
• Ex of stimulatory?
  1. ) Myastheria gravis: Ab against? Type of damage? Mediated by?
  2. ) Rheumatic fever: Occurs after? Ab’s attack what?
  3. ) Dresslers Syndrome: Occurs when? What is attacked?
  4. ) Good Pasture Disease: Ab attacks what? Then what happens?
  5. ) Autoimmune thrombocytopenia: Ptts opsonized by? Picked up by? What then happens?
  6. ) AIHA: Two types?
  7. ) Lupus: Ab against? (4) May lead to?
  8. ) Hashimoto: Inflamm. disease of? Leads to?
  9. ) Graves Disease: IgG binds what? Leads to?

Answer 5

• Antibodies; own tissues or cells
• Binds TSR leading to hyperthyroidism
• Ach receptor; primary; neut/compliment mediated
• Strep pyrogenes infection; laminin in heart valve
• post heart attack; pericardium
• Ab to type 4 collagen on BM of lung/kidney; many things go into kidney
• Ab; picked up by spleen and excess bleeding
• Warm and cold
• Nuclear/nucleolar proteins, DNA, RNA, butterfly rash
• Thyroid; T and B cell attack and hypothyroid
• IgG binds TSH receptor leading to hyperthyroidism

Question 6

Type 2 Immunopathology:

• Flourescent test for good pasture disease: Direct? Indirect? Linear pattern suggests? Lumpy-Bumpy suggests?
• Autoimmune Disease from:
  1. ) Innocent bystander: Def? Ex?
  2. ) Cross reaction: Def? Ex?
  3. ) Coupling: Def?
  4. ) Forbidden clone: Def? Ex?
  5. ) Exposure to sequestered antigen: Def? Ex?
  6. ) Failure of T-reg: Def?
• AIRE gene: Cause what? Help T cells do what?

Answer 6

• Take kidney and add goats IgG
• Normal kidney then add patients IgG then goats IgG; Good Pasture; Lupus
  1. ) Attack an infection and killing local tissue, TB
  2. ) Ab for one antigen with increased affinity for own tissue; R. Fever
  3. ) B cell binds own protein and shows to T cells
  4. ) Clone escapes detection; M. Gravis
  5. ) Immune cells getting where they shouldn’t; Blood teste barrier
  6. ) Low Treg levels
• Stromal thymic to express wide range of genes; know self

Question 7

Type 4 Immunopathology:

• Mediated by? Delayed what? Require B cells? But?
• Steps to poison ivy example?
• How does TB (mantoux) test work? Can have positive test with?
• What can happen with small peptides?
• How can T cell response be measured in vitro?
• Why can TB test be used multiple times?

Answer 7

• T cells; hypersensitivity; no; but usually does
• Exposed to urushoil oil (penetrates skin), assoc. with MH2 on DC’s; TH1/TH17’s develop, now immunized but antigen washed off, reencounter the oil, memory cells respond, IFN gamma released, MACs come in; this is due to lower threshold
• Small amount of purified TB added, TB taken to local DCs, If memory cells exist then response ensues; Bacille-Calmette vaccine (Bovine)
• May act as epitope for MHC leading to response
• Whole blood incubated with antigen to see cell proliferation and cytokine release; won’t respond to Bovine version
• PPD dose too low to make memory cells

Question 8

Type 4 Immunopathology:

1. ) First set rejection?
2. ) Second set rejection? Due to? What if completely new donor is used?
3. ) Hyperacute rejection (white graft): Occurs? Ab’s against? Often occurs with? Why?
   - Autoimmunity to environmental exposure: Ex: Brain: Antigenic? Immunogenic? Why? Do anti brain T cells exist? Example where this happens? Similar to?
   - 3 parts to Graft vs. host?
   - Graft vs. Leukemia: Good thing?
   - How can HLA play role in autoimmunity?

Answer 8

1. ) Recipient rejects graft after a while due to 5-10% T cells recognize graft MHC as self MHC
2. ) Another graft creates faster response; memory cells; no quick response
3. ) Almost immediately; histocompatibility antigens; xenografts; pre exisiting ab’s for other species
   - Yes; no; not presented to t cells during development; yes; Meat packers; MS
   - graft contains immunocompetent t cells; host has antigen that graft t cells recognize; host immunocompromised
   - yes
   - Arrangement of AA’s make them likely to pick up self protein