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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. What are target cells?
Cells that stil have weird parts of their membrane that macrophages usually bite off
cannot cross placenta
Not thymus - BM
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

2. What does interferon gamma do to be antiviral?
TLR ad nuclear receptors
Viral neutralization of igM and IgG!
Increases expression of MHC I and MHC II and also activates NK cells
Anti viral and anti tumor

3. What is a factor that is a predictor for a bad transplantation?
Type IV
IgA
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
No because no peptide fragment!

4. What is recomb beta interferon used for?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
MS
If there is class switching and plasma cell production (that is when memory cells are produced)
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. can igG cross the placenta?
neutrophilia!
Yes
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Viral neutralization of igM and IgG!

6. The MALT/GALT are not...
Influenza; antigenic shift; antigenic drift
encapsulated
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
2 heavy chains and two light chains

7. What is the receptor for EBV? On what cells is that located?
Liver! (they are proteins circulating in the blood)
pentamer
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Fc

8. What is the marginal zone of the spleen? what happens there?
2 heavy chains and two light chains
Edema and necrosis in that region
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
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

9. Which MHC presents intracellular peptides? how so?
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
CRP - C3b - IgM
MHC I; from RER with help of the B2 microglobulin
Fc

10. What is the pathogenesis of a hypersensitivity reaction?
Anti mitochondrial
Activates Th1 helper cells; Macrophages
DM type I
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

11. 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
Secretory component
Negative nitroblue tetrazolium reduction test
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

12. What is the common variable immunodeficiency ? How is it different from Brutons?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
A recomb cytokine of IL 2; RCC and metastatic melanoma
Superior mesenteric
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

13. IgM can fix complement but...
Anti mitochondrial
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Anemias (esp due to renal failure)
cannot cross placenta

14. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Immunoflourescent staining of tissue biopsies
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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

15. The ______ in the BM are DN - the DP are in the cortex of thymus
Antimicrosomal and antithyroglobulin
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
T cell precursor
DM type I and RA

16. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
IgE
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti viral and anti tumor

17. How is the thymus organized? what happens in each section?
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
Delayed type hypersensitivity
Activates cytotoxic CD 8 T cells as second signal
Th2; Th1

18. How fast does it occur?
Activate macrophages
C5a
The patient could become cyanotic in the OR!
Superficial inguinal

19. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
A - B - C; all the D's
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
When you select for which MHC it will have; take out the lymphs that self react
Internal iliac

20. where are complements produced?
Paracortex
Liver! (they are proteins circulating in the blood)
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
Anti IF

21. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
SP infections
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

22. 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)
Alternative splicing of mRNA
Kill them because they have CD16 on them that recognize the FcG portion
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

23. For which toxins are preformed antibodies (passive) given?
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Tetanus - Botulinum - HBV - Rabies

24. T/F B cells do not require a second signal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IgA
False! B cell class switching requires a second signal

25. What happens in a secondary follicle?
If there is class switching and plasma cell production (that is when memory cells are produced)
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

26. 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!
Anti mitochondrial
Steroid responsive nephrotic syndrome
not Ab mediated

27. What is anergy? why does this occur?
IgE; by activating eosinophils
Para aortic
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
active complement pathway

28. Which diseases are associated with DR4?
Superficial inguinal
DM type I and RA
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
Not thymus - BM

29. What is the presentation of common variable immunodef? and What are the labs?
heavy chains
Axillary
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
Barrel hoop basement membrane fenestrations

30. What is the defect in hyper IgM syndrome? What are the lab results?
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
A - B - C; all the D's
...
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

31. hat is the presentation of Jobs syndrome or Hyper IgE?
encapsulated
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Graves
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

32. What is the autoantibody for SLE that is nonspecific? Specific?
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

33. What is oprelevkin? and What is it used for?
Antidesmoglein
Superficial inguinal
Recom IL 11; thrombocytopenia
neutrophilia!

34. Other than stimulating fever - what else does IL 6 do?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Stimulate the liver to release acute phase reactants
secondary
Acts as second signal on B cells to induce class switching to IgE and IgG

35. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
secondary
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

36. Give three examples of bacteria that use antigenic variation and how.
lowest concentration
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

37. What are the function of B cells?
Active; passive - fast but short half life (3 weeks!)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

38. What does IgA pick up from epithelial cells before being secreted?
Its a serine protease that activates apoptosis; NK and CD8
Secretory component
...
cannot cross placenta

39. what mediates the type II hypersensitivity? What are the two different methods?
IgG
Antibody mediated cytotoxicity; either complement dependent or complement independent
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

40. What are the three types of lymphocytes?
B - T - and NK cells
T cell activation; no with CD 4 or CD 8
All MHC 1/CD8
Fab portion

41. What does Interferon alpha and beta do? how?
Superficial inguinal
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

42. What type of fenestrations are found in the red pulp of the spleen?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Barrel hoop basement membrane fenestrations
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

43. What is digoxin immune Fab used for?
MS
Delayed type hypersensitivity
IgM
Antidote for digoxin intoxication

44. So antibodies are the effectors for the humoral response. List some of their functions.
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
Receiving preformed Antibodies
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

45. What is the general structure of an Ab?
2 heavy chains and two light chains
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Daclizumab; prevent ACUTE rejection of renal transplant
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

46. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
mesenchymal
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Recom IL 11; thrombocytopenia
IgG

47. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
...
Macrophages - Dendritic cells - B cells
Immunoflourescent staining of tissue biopsies

48. What are the autoantibodies for pemphigus bulgaris?
Lymphocytes
IgG
Antidesmoglein
TGF beta and IL 10

49. What are the main Cell surface proteins on T cells?
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
T cell dysfunction
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

50. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
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
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic