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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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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 autoantibodies for drug induced lupus?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Antihistone
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Activate macrophages

2. What lymph node drains the scrotum?
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Rheumatic arthritis
Superficial inguinal

3. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
except hyperacute
Remove encapsulated bacateria
Its main effect is a defect in Ab opsonization for killing
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(

4. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
SP infections
Anti alpha subunit 3 of collagen on type IV bm
All MHC 1/CD8

5. what secretes IL 4?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IgM and IgD
Basophils! THey want IG E class switch!
T cell precursor

6. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Its main effect is a defect in Ab opsonization for killing
Remove encapsulated bacateria

7. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Rheumatic arthritis
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Type IV

8. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
C5a
In the germinal center of secondary follicles (In the paler center)
Anti IF

9. What are the autoantibodies for graves?
Cross link
The patient could become cyanotic in the OR!
Anti TSh receptor
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

10. which type of immunity is slow but long lasting? as opposed to...
...
Humoral
Active; passive - fast but short half life (3 weeks!)
Negative selection

11. What is the clinical use of Muromonab?
Macrophages - Dendritic cells - B cells
Immunosuppression after kidney transplantation
Anemias (esp due to renal failure)
Active; passive - fast but short half life (3 weeks!)

12. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Interferon gamma; Th1
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

13. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Cross link
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

14. T/F B cells do not require a second signal
CD56
False! B cell class switching requires a second signal
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
2 heavy chains and two light chains

15. What are the two signals required for Th1 cells? what happens after then activated?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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
encapsulated
Hereditary angioedema; PNH

16. Other than stimulating fever - what else does IL 6 do?
Give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
MS
Stimulate the liver to release acute phase reactants

17. What is Aldesleukin? What is it used for
Steroid responsive nephrotic syndrome
Graves
A recomb cytokine of IL 2; RCC and metastatic melanoma
Axillary

18. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Celiac

19. What is hereditary angioedema? What are the C3 levels?
T cell precursor
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
Bind FcG for antibody dependent cellular cytotoxicity
DM type I

20. What is colostrum?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
MHC I - CD16 - CD56
Chronic granulomatous disease
The igA found in breast milk

21. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Lymphocytes
Negative nitroblue tetrazolium reduction test
Basophils! THey want IG E class switch!

22. in which immunodef order do you see a lot of pus? no pus?
Hemochromatosis
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IL 4 - 5 - 10 - 6
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

23. IgE has the ___________ in the serum
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
lowest concentration
IL 3; supports growth and differentiation of bone marrow stem cells
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

24. Monomer in circulation - ___ when secreted
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Influenza; antigenic shift; antigenic drift
IL 4 - 5 - 10 - 6
dimer

25. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Antidesmoglein
Humoral
Anti SS- A (anti RO) and Anti SS- B

26. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
MS - hay fever - SLE - goodpastures
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

27. can igG cross the placenta?
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Yes
RNA segment reassortment

28. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
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
Negative!
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

29. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Viral neutralization of igM and IgG!

30. Leukocyte adhesion defect presents with...
neutrophilia!
carboxy terminal
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia

31. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Activates cytotoxic CD 8 T cells as second signal
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

32. What does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
Negative selection
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

33. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
delayed!
TNF alpha and IL1
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

34. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
opsonizes
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Cyclosporine - OKT3

35. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
CRP - C3b - IgM
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

36. What is the treatment of acute transplant rejection?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
CRP - C3b - IgM
Cyclosporine - OKT3
Popliteal

37. The MALT/GALT are not...
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
encapsulated
Anemias (esp due to renal failure)

38. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
except hyperacute
Paracortex; viral infection
MHC I; from RER with help of the B2 microglobulin
IL 5

39. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

40. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti Ach receptor
T cell dysfunction

41. 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)
Cytokine IL 10 secreted by Th2
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

42. What lymph node drains the upper limb?
Activates cytotoxic CD 8 T cells as second signal
Axillary
Superficial inguinal
Interferon gamma; Th1

43. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Immunosuppression after kidney transplantation
Th cells fail to produce interferon gamma; a lot of IgE
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
Basophils! THey want IG E class switch!

44. what cell surface marker is used for NK cells as it is unique to them?
CD56
Paracortex
Cytokine IL 10 secreted by Th2
Superior mesenteric

45. What do multimeric antibodies require for assembly?
A j chain
...
Remove encapsulated bacateria
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

46. 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?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
NK cells
active complement pathway
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

47. What are the autoantibodies for pemphigus bulgaris?
Antidesmoglein
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti smooth muscle

48. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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

49. What are the autoantibodies for hashimotos?
Popliteal
Anti viral and anti tumor
Antimicrosomal and antithyroglobulin
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

50. describe the pathogenesis of delayed type IV hypersensitivity
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
2 heavy chains and two light chains

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USMLE Step 1 Immunology

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