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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. The Fc region is found on the...
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
carboxy terminal
Influenza; antigenic shift; antigenic drift
S. aureus - E. Coli - aspergillus

2. where are complements produced?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Liver! (they are proteins circulating in the blood)

3. The lymphocytes are ________ origin
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
mesenchymal

4. Which antibodies can be multimeric?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgM and IgA
Th cells fail to produce interferon gamma; a lot of IgE

5. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
A j chain
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Antibody mediated cytotoxicity; either complement dependent or complement independent
IgE; by activating eosinophils

6. What lymph node drains the anal canal (below the pectinate line)?
When you select for which MHC it will have; take out the lymphs that self react
Superficial inguinal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

7. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Internal iliac
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Alternative splicing of mRNA

8. What is the marginal zone of the spleen? what happens there?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
Acts as second signal on B cells to induce class switching to IgE and IgG
Tetanus - Botulinum - HBV - Rabies

9. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
RNA segment reassortment
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Paracortex

10. What are target cells?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
A chemotactic factor for neutrophils
Cells that stil have weird parts of their membrane that macrophages usually bite off

11. What is the general structure of an Ab?
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
2 heavy chains and two light chains
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

12. Leukocyte adhesion defect presents with...
IgG
Humoral
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
neutrophilia!

13. What are howell jolly bodies?
DM type I
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

14. What cytokines to Th2 secrete?
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 4 - 5 - 10 - 6
Superficial inguinal

15. Which type of selection of thymic development provides central tolerance?
Rheumatic arthritis
Negative selection
not Ab mediated
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

16. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Fab portion
MHC class molecules bind to KIRS or CD94 to prevent killing
MS

17. T/F B cells do not require a second signal
Superior mesenteric
If there is class switching and plasma cell production (that is when memory cells are produced)
False! B cell class switching requires a second signal
Active; passive - fast but short half life (3 weeks!)

18. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
CD56
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
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

19. What is the most common selective Ig deficiency? What is the presentation?
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
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
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 TSh receptor

20. what happens in a deficiency of C1 esterase inhibitor? DAF?
Hereditary angioedema; PNH
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
If there is class switching and plasma cell production (that is when memory cells are produced)

21. What does IL 4 do?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Acts as second signal on B cells to induce class switching to IgE and IgG
Activate macrophages
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

22. What is the main function of TNF alpha? How does it do this?
RNA segment reassortment
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Negative selection
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

23. 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?
Interferon gamma; Th1
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Antibody mediated cytotoxicity; either complement dependent or complement independent
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

24. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Antidesmoglein
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

25. Give three examples of bacteria that use antigenic variation and how.
Bind FcG for antibody dependent cellular cytotoxicity
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Activates Th1 helper cells; Macrophages
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

26. What is hereditary angioedema? What are the C3 levels?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
CRP - C3b - IgM
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
Anti glutamate carboxylase and anti insulin

27. What does CD16 on NK cells do?
IgG
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
Bind FcG for antibody dependent cellular cytotoxicity

28. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
pentamer
IL 5
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

29. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
Macrophages - Dendritic cells - B cells
CD56
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

30. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Negative selection
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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

31. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Anti viral and anti tumor
Negative nitroblue tetrazolium reduction test
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Liver! (they are proteins circulating in the blood)

32. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Activate macrophages
Activates cytotoxic CD 8 T cells as second signal
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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)

33. What are the autoantibodies for pemphigus bulgaris?
Superficial inguinal
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
When you select for which MHC it will have; take out the lymphs that self react
Antidesmoglein

34. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
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
Anemias (esp due to renal failure)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Paracortex; viral infection

35. What type of side chains are found on Fc region of an antibody?
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
Immunoflourescent staining of tissue biopsies
Carbohydrate
IgE

36. What is a factor that is a predictor for a bad transplantation?
mesenchymal
Basophils! THey want IG E class switch!
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
MHC I; from RER with help of the B2 microglobulin

37. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Sinusitis - otitis media - pneumonia
...
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

38. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Sinusitis - otitis media - pneumonia
S. aureus - E. Coli - aspergillus
Its main effect is a defect in Ab opsonization for killing
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

39. hat is the presentation of Jobs syndrome or Hyper IgE?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
B - T - and NK cells
Th2; Th1
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

40. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
The patient could become cyanotic in the OR!
By transcytosis
...

41. what cell surface proteins are on all APCs?
dimer
IL 3; supports growth and differentiation of bone marrow stem cells
MHC II - B7
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

42. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its main effect is a defect in Ab opsonization for killing
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

43. Which is the main antibody in the delayed or secondary response to an antigen?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Superficial inguinal
IgG
Lymphocytes

44. Which disease is associated with HLA A3?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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
Hemochromatosis
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

45. IgM can fix complement but...
Superficial inguinal
MS
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
cannot cross placenta

46. What is the presentation of Brutons agammaglobulinemia?
Cells that stil have weird parts of their membrane that macrophages usually bite off
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Superficial inguinal

47. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
T cell dysfunction
Sinusitis - otitis media - pneumonia
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

48. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Anti Jo -1
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
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

49. What is chronic mucocutaneous candidiasis d/t?
Paracortex
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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
T cell dysfunction

50. What is the main function of interferons?
Acts as second signal on B cells to induce class switching to IgE and IgG
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Alternative splicing of mRNA
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)