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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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. How is sirolimus different from tacrolimus?
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Previous transfusion; pregnant woman whose fetus had paternal antigens
T

2. What does interferon gamma do to be antiviral?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Increases expression of MHC I and MHC II and also activates NK cells
Hereditary angioedema; PNH
Para aortic

3. What are the autoantibodies for wegeners granulomatosis?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

4. What are the two signals to kill for NK cells?
cannot cross placenta
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

5. 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?
IgE; by activating eosinophils
Receiving preformed Antibodies
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
except hyperacute

6. hat is the presentation of Jobs syndrome or Hyper IgE?
RNA segment reassortment
Anti viral and anti tumor
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

7. 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)
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
secondary
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)

8. Which disease is associated with DR7?
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Steroid responsive nephrotic syndrome

9. How do you test for type III hypersensitivity?
DM type I
C5a
Immunoflourescent staining of tissue biopsies
IgM and IgD

10. The Fc region is found on the...
Negative nitroblue tetrazolium reduction test
Basophils! THey want IG E class switch!
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

11. What is the pathogenesis of HyperIgE syndrome? What are the labs?
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
Th cells fail to produce interferon gamma; a lot of IgE
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
All MHC 1/CD8

12. What lymph node drains the upper limb?
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
Axillary

13. The ______ in the BM are DN - the DP are in the cortex of thymus
Remove encapsulated bacateria
Superficial inguinal
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
T cell precursor

14. what happens in a deficiency of C1 esterase inhibitor? DAF?
Hereditary angioedema; PNH
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

15. What are the autoantibodies for polymyositis and dermatomyositis?
B - T - and NK cells
Anti Jo -1
If there is class switching and plasma cell production (that is when memory cells are produced)
Cytokine IL 10 secreted by Th2

16. What does IL 2 do?
Wiskott Aldrich syndrome
Stimulate the liver to release acute phase reactants
Activates cytotoxic CD 8 T cells as second signal
Yes

17. __________ are a part of the innate system.
Graves
CRP - C3b - IgM
NK cells
Anemias (esp due to renal failure)

18. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Superior mesenteric
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
MS - hay fever - SLE - goodpastures
IgG

19. what ensure that a memory response is generated?
TLR ad nuclear receptors
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
If there is class switching and plasma cell production (that is when memory cells are produced)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

20. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Anti Ach receptor
carboxy terminal
When you select for which MHC it will have; take out the lymphs that self react

21. Which disease is associated with DR3?
2 heavy chains and two light chains
DM type I
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
carboxy terminal

22. What is the main function of interferons?
Yes
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
DM type I
Receiving preformed Antibodies

23. How is i Th1 helper cell inhibited?
Cytokine IL 10 secreted by Th2
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Paracortex
dimer

24. What is the main cytokine released by T cells? What does it do
encapsulated
Stimulate the liver to release acute phase reactants
IL 3; supports growth and differentiation of bone marrow stem cells
pentamer

25. Which disease is associated withB B27?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
CRP - C3b - IgM

26. Describe complement dependent Type II hypersensitivity. Give an example.
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Interferon gamma; Th1
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)

27. To what portion of the Antibody do the complements bind?
Wiskott Aldrich syndrome
Daclizumab; prevent ACUTE rejection of renal transplant
Fc
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

28. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
heavy chains
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
...
Wiskott Aldrich syndrome

29. what cell surface marker is used for NK cells as it is unique to them?
CD56
Sinusitis - otitis media - pneumonia
Local infection/inflammation; infection of the ln itself; metastasis
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

30. What is filgrastim and sargramostim? and What is it used for?
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
pentamer
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Antidote for digoxin intoxication

31. What is muromonab - CD3 (OKT3)
Anti smooth muscle
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

32. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Antibody mediated cytotoxicity; either complement dependent or complement independent
Activate macrophages
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

33. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Barrel hoop basement membrane fenestrations

34. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Fc
MS - hay fever - SLE - goodpastures
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

35. where do NK cells develop?
Not thymus - BM
Secretory component
Cyclosporine - OKT3
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)

36. What is the most common selective Ig deficiency? What is the presentation?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
...
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

37. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
Anti IF
When you select for which MHC it will have; take out the lymphs that self react
False! B cell class switching requires a second signal

38. what characterizes an arthus reaction?
Humoral
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
Edema and necrosis in that region
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

39. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
RNA segment reassortment
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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

40. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Activates Th1 helper cells; Macrophages
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Influenza; antigenic shift; antigenic drift

41. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
IgA
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
DM type I

42. What is oprelevkin? and What is it used for?
C5a
Recom IL 11; thrombocytopenia
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

43. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
NK cells
S. aureus - E. Coli - aspergillus
DM type I and RA

44. what will NK cells do to cells covered in IgG Ab? why?
IgG
Kill them because they have CD16 on them that recognize the FcG portion
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
DM type I

45. 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?
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
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
carboxy terminal

46. What lymph node drains the scrotum?
Superficial inguinal
IgE; by activating eosinophils
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Edema and necrosis in that region

47. What are the main symptoms of T cell immunodeficiencies?
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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 :(
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

48. What are the autoantibodies for pernicious anemia?
Anti IF
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
SP infections
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

49. Name the three opsonins
CRP - C3b - IgM
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Cyclosporine - OKT3

50. Which antibodies can be multimeric?
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
IgM and IgA
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Recom IL 11; thrombocytopenia