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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 happens in a secondary follicle?
Barrel hoop basement membrane fenestrations
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Celiac
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

2. What is digoxin immune Fab used for?
Barrel hoop basement membrane fenestrations
Antidote for digoxin intoxication
When you select for which MHC it will have; take out the lymphs that self react
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

3. which antibody is involved in the primary response or immediate response to an antigen?
Antibody mediated cytotoxicity; either complement dependent or complement independent
A - B - C; all the D's
Its a serine protease that activates apoptosis; NK and CD8
IgM

4. which cytokine inhibits TH2 cells? secreted by who?
Influenza; antigenic shift; antigenic drift
Cross link
CRP - C3b - IgM
Interferon gamma; Th1

5. How does complement link innate and adaptive?
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
2 heavy chains and two light chains
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

6. other than C3a - what other complement acts as an anaphyloxin?
Celiac
C5a
Kill them because they have CD16 on them that recognize the FcG portion
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

7. In general What are T cells good for?
Pernicious Anemia and Hashimotos
Anti viral and anti tumor
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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

8. How do you test for chronic granulomatous disease?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Pernicious Anemia and Hashimotos
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Negative nitroblue tetrazolium reduction test

9. How is i Th1 helper cell inhibited?
Negative nitroblue tetrazolium reduction test
The igA found in breast milk
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Cytokine IL 10 secreted by Th2

10. what will NK cells do to cells covered in IgG Ab? why?
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Hereditary angioedema; PNH
Kill them because they have CD16 on them that recognize the FcG portion

11. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
IgM and IgG
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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

12. The idiotype; the Fc portion determines the...
IgM
IL 5
Anti Ach receptor
isotype

13. What are MHC's necessary for? By themselves?
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
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
T cell activation; no with CD 4 or CD 8
Cross link

14. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Graves
Yes
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 :(
Edema and necrosis in that region

15. which antibody activate mast cells - basophils - and eosinophils?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Delayed type hypersensitivity
IgE
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen

16. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Complement activation (active in both)
All MHC 1/CD8
SP infections
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

17. What does IL 2 do?
Lymphocytes
Inferior mesenteric
Complement activation (active in both)
Activates cytotoxic CD 8 T cells as second signal

18. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Cross link
Pernicious Anemia and Hashimotos
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

19. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

20. 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
neutrophilia!
Acts as second signal on B cells to induce class switching to IgE and IgG
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

21. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
IL 3; supports growth and differentiation of bone marrow stem cells
type four
Its main effect is a defect in Ab opsonization for killing
except hyperacute

22. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
Cytokine IL 10 secreted by Th2
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IL 15; IL 12 - interferon Beta and interferon alpha

23. what cell surface marker is used for NK cells as it is unique to them?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anemias (esp due to renal failure)
CD56
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

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)
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)
Anti U1 RNP (ribonucleoprotein)
Interferon gamma and IL 2

25. What are the two signals required for T cells? what happens after?
NK cells
Remove encapsulated bacateria
The igA found in breast milk
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

26. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

27. What are the major functions of Antibodies?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
IL 1 and IL 6
Th2; Th1
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

28. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IgG
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

29. What type of side chains are found on Fc region of an antibody?
Carbohydrate
Humoral
heavy chains
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

30. IgM can fix complement but...
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
cannot cross placenta

31. 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
active complement pathway
Bind FcG for antibody dependent cellular cytotoxicity
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep

32. What links the adaptive and innate immunity?
Complement activation (active in both)
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
Fab portion

33. What are the symptoms of serum sickness?
Negative selection
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

34. How does the alternative pathway lead to MAC activation?
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
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
A chemotactic factor for neutrophils
Recom IL 11; thrombocytopenia

35. What is a factor that is a predictor for a bad transplantation?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
pentamer
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
...

36. What is the main function of interferons?
active complement pathway
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
Receiving preformed Antibodies
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

37. What type of fenestrations are found in the red pulp of the spleen?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Pernicious Anemia and Hashimotos
Barrel hoop basement membrane fenestrations

38. What are the three types of APCs?
Hemochromatosis
C5a
Macrophages - Dendritic cells - B cells
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

39. What is the defect in hyper IgM syndrome? What are the lab results?
Stimulate the liver to release acute phase reactants
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
The igA found in breast milk

40. What are the autoantibodies for drug induced lupus?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Antihistone
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

41. What does IL 5 do?
Paracortex; viral infection
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
NK cells

42. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
IL 5

43. What is the presentation of scid? treatment?
Barrel hoop basement membrane fenestrations
Delayed type hypersensitivity
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
MHC II - B7

44. Which diseases are associated with DR5?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Barrel hoop basement membrane fenestrations
Pernicious Anemia and Hashimotos

45. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
pathogenesis
Popliteal
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

46. The alternative pathway is the only constutively...
IgG
Liver! (they are proteins circulating in the blood)
No because no peptide fragment!
active complement pathway

47. which B and T cell disorder presents with specifically low IgM?
mesenchymal
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
Wiskott Aldrich syndrome
Anti alpha subunit 3 of collagen on type IV bm

48. The pathogenesis of contact dermatitis is ________ hypersensitivity
neutrophilia!
type four
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IL 3; supports growth and differentiation of bone marrow stem cells

49. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
isotype
Anti Ach receptor
RNA segment reassortment
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

50. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Th2; Th1
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Pernicious Anemia and Hashimotos
TNF alpha and IL1