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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.

This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.

1. What are the two signals required for T cells? what happens after?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

2. which cells have more complete tolerance - B or T cells?
Axillary
T
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Daclizumab; prevent ACUTE rejection of renal transplant

3. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
dimer
not Ab mediated
Macrophages - Dendritic cells - B cells

4. How does the alternative pathway lead to MAC activation?
TLR ad nuclear receptors
Fab portion
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II

5. Give three examples of bacteria that use antigenic variation and how.
MHC II - B7
Cytokine IL 10 secreted by Th2
...
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

6. What is recomb beta interferon used for?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IgA
MS
Histamine; post capillary venules - vasodilation

7. which antibodies can bind complement?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgM and IgG
Cells that stil have weird parts of their membrane that macrophages usually bite off
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs

8. what results in symptoms of shock in an acute hemolytic transfusion reaction?
A chemotactic factor for neutrophils
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Remove encapsulated bacateria
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

9. give an example of how influenza does a major antigenic shift.
IgM
RNA segment reassortment
acute phase reactants
Antidesmoglein

10. What is the treatment of acute transplant rejection?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Cyclosporine - OKT3
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!

11. What are the autoantibodies for primary biliary cirrhosis?
MHC class molecules bind to KIRS or CD94 to prevent killing
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti mitochondrial
Barrel hoop basement membrane fenestrations

12. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Interferon gamma and IL 2
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

13. What does IL 5 do?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Previous transfusion; pregnant woman whose fetus had paternal antigens
not Ab mediated

14. What is recomb alpha interferon used for?
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

15. What are the cell surface proteins on NK cells?
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Humoral
MHC I - CD16 - CD56
Axillary

16. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Tetanus - Botulinum - HBV - Rabies
...
encapsulated

17. when can graft versus host disease? What is the result?
Basophils! THey want IG E class switch!
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
NK cells
Fab portion

18. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Antimicrosomal and antithyroglobulin
C5a
RNA segment reassortment

19. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
MHC I; from RER with help of the B2 microglobulin
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

20. Which diseases are associated with DR4?
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
DM type I and RA
A - B - C; all the D's
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

21. What is oprelevkin? and What is it used for?
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
Edema and necrosis in that region
Basophils! THey want IG E class switch!
Recom IL 11; thrombocytopenia

22. What is three common causes of severe combined immunodef? What is the result of all three?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Th cells fail to produce interferon gamma; a lot of IgE
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

23. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Superficial inguinal
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Rheumatic arthritis
Influenza; antigenic shift; antigenic drift

24. What are the three types of lymphocytes?
Anti glutamate carboxylase and anti insulin
B - T - and NK cells
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
CD21 on B cells (although there is T cell lymphocytosis in EBV)

25. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Celiac
secondary
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

26. What cytokines are released by Th1 cells?
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
Interferon gamma and IL 2
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
Anti U1 RNP (ribonucleoprotein)

27. What does it mean if there are igM in the serum at birth?
IgA
By transcytosis
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

28. What are the autoantibodies for myasthenia gravis?
Anti viral and anti tumor
Anti Ach receptor
Lymphocytes
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

29. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Acts as second signal on B cells to induce class switching to IgE and IgG
A j chain
Antidesmoglein
TNF alpha and IL1

30. Which diseases are associated with DR2?
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
MS - hay fever - SLE - goodpastures
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Activates Th1 helper cells; Macrophages

31. What does granulysin do?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Receiving preformed Antibodies
Cytokine IL 10 secreted by Th2

32. Which disease is associated with DR7?
Hemochromatosis
Steroid responsive nephrotic syndrome
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

33. __________ are a part of the innate system.
Thrombocytopenia
NK cells
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Superficial inguinal

34. Which antibody mediates immunity to worms? how?
Severe pyogenic infections early in life
Wiskott Aldrich syndrome
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
IgE; by activating eosinophils

35. what cell surface proteins are on all APCs?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
MHC II - B7

36. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
IL 5
encapsulated
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
If there is class switching and plasma cell production (that is when memory cells are produced)

37. which of the transplant rejections is antibody mediated? why does it occur?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
DM type I and RA
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

38. From where do cytokines come from?
Lymphocytes
The igA found in breast milk
Hereditary angioedema; PNH
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

39. What do mature naive B lymphocytes express?
Para aortic
IgM and IgD
Fab portion
IgM and IgG

40. What are the mediators that mast cells release?
All MHC 1/CD8
Antidesmoglein
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

41. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
A j chain
Lymphocytes

42. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Anti TSh receptor
Interferon gamma; Th1

43. where are complements produced?
Active; passive - fast but short half life (3 weeks!)
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
Liver! (they are proteins circulating in the blood)
Cells that stil have weird parts of their membrane that macrophages usually bite off

44. which of the hypersensitivity reactions is not Ab mediated?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgG
Type IV
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

45. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
Interferon gamma and IL 2
Severe pyogenic infections early in life
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

46. What are the cell surface proteins for Macrophages? which two are for opsonins?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
...

47. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
C5a
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Kill them because they have CD16 on them that recognize the FcG portion
Anemias (esp due to renal failure)

48. What does IgA pick up from epithelial cells before being secreted?
C5a
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
Secretory component
DM type I

49. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Thrombocytopenia
MHC II - B7

50. what secretes IL 4?
IL 4
Basophils! THey want IG E class switch!
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp