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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
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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. Describe the Mannose Lectin pathway
Active; passive - fast but short half life (3 weeks!)
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
Fc
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway

2. The MALT/GALT are not...
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Axillary
encapsulated
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

3. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

4. in which immunodef order do you see a lot of pus? no pus?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Superficial inguinal
No because no peptide fragment!
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

5. What happens in a deficiency of C3?
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
lowest concentration

6. The idiotype; the Fc portion determines the...
Chronic granulomatous disease
isotype
neutrophilia!
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d

7. Name two endogenous pyrogens
IL 1 and IL 6
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Inferior mesenteric

8. Which disease is associated with B8?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Graves
Remove encapsulated bacateria
Hemochromatosis

9. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Anti glutamate carboxylase and anti insulin
Cross link

10. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
carboxy terminal
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
pathogenesis
B - T - and NK cells

11. What is the presentation of scid? treatment?
CD56
Popliteal
acute phase reactants
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

12. where are complements produced?
Its main effect is a defect in Ab opsonization for killing
Complement activation (active in both)
Liver! (they are proteins circulating in the blood)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

13. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
TGF beta and IL 10
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
MHC I - CD16 - CD56
Antihistone

14. In thymic development - What is the positive selection? negative selections?
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
When you select for which MHC it will have; take out the lymphs that self react

15. What is hereditary angioedema? What are the C3 levels?
Antibody mediated cytotoxicity; either complement dependent or complement independent
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx

16. ________ regulate the cell mediated response.
Humoral
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
cannot cross placenta

17. What is Aldesleukin? What is it used for
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Superficial inguinal
A recomb cytokine of IL 2; RCC and metastatic melanoma
B - T - and NK cells

18. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
A - B - C; all the D's

19. What are howell jolly bodies?
MS
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway

20. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Hemochromatosis
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

21. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
...
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Rheumatic arthritis

22. What does interferon gamma do? What two type of cells does it attack mostly?
Secretory component
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
lowest concentration
Chronic granulomatous disease

23. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti topoisomerase
Internal iliac
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

24. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
MHC I - CD16 - CD56
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Cytokine IL 10 secreted by Th2

25. Complements are...
IgE; by activating eosinophils
acute phase reactants
Antihistone
mesenchymal

26. which B and T cell disorder presents with specifically low IgM?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Wiskott Aldrich syndrome
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
The patient could become cyanotic in the OR!

27. What are the main Cell surface proteins on T cells?
Negative!
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Steroid responsive nephrotic syndrome
Lymphocytes

28. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Carbohydrate
Hemochromatosis
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

29. What is the presentation of hyperIgM syndrome?
isotype
Previous transfusion; pregnant woman whose fetus had paternal antigens
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Severe pyogenic infections early in life

30. What is the defect in hyper IgM syndrome? What are the lab results?
Bind FcG for antibody dependent cellular cytotoxicity
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi

31. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
CRP - C3b - IgM
Alternative splicing of mRNA
pathogenesis
Daclizumab; prevent ACUTE rejection of renal transplant

32. What is the pathology in hyperacute transplant rejection?
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
CD56
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Secretory component

33. what cell surface marker is used for NK cells as it is unique to them?
IgAs in mothers breast milk!
pentamer
IL 4 - 5 - 10 - 6
CD56

34. What is thrombopoietin used for?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Popliteal
Thrombocytopenia
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

35. T/F B cells do not require a second signal
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
dimer
False! B cell class switching requires a second signal
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

36. which antibody activate mast cells - basophils - and eosinophils?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Previous transfusion; pregnant woman whose fetus had paternal antigens
IgE

37. Which antibody mediates immunity to worms? how?
Receiving preformed Antibodies
Anti TSh receptor
Superior mesenteric
IgE; by activating eosinophils

38. What are the autoantibodies for primary biliary cirrhosis?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Anti mitochondrial
encapsulated
Cyclosporine - OKT3

39. IgE has the ___________ in the serum
Daclizumab; prevent ACUTE rejection of renal transplant
cannot cross placenta
Anti Ach receptor
lowest concentration

40. Describe the capsular structure of a lymph node; What are the functions of the LN?
Antidesmoglein
MHC I - CD16 - CD56
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

41. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Superficial inguinal
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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

42. What are the autoantibodies for myasthenia gravis?
encapsulated
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti Ach receptor
Fc

43. What lymph node drains the breast?
Anemias (esp due to renal failure)
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Axillary

44. So antibodies are the effectors for the humoral response. List some of their functions.
Its main effect is a defect in Ab opsonization for killing
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
TGF beta and IL 10

45. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti TSh receptor
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

46. What is muromonab - CD3 (OKT3)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Basophils! THey want IG E class switch!
Stimulate the liver to release acute phase reactants

47. What are the mediators that mast cells release?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
The igA found in breast milk
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

48. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
C5a
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

49. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
Influenza; antigenic shift; antigenic drift
Cells that stil have weird parts of their membrane that macrophages usually bite off
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig

50. What is recomb gamma interferon used for?
Liver! (they are proteins circulating in the blood)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Chronic granulomatous disease
MHC I - CD16 - CD56

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USMLE Step 1 Immunology

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