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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 is the main function of IL 8?
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
Active; passive - fast but short half life (3 weeks!)
pale central germinal centers
A chemotactic factor for neutrophils

2. what cytokine does basophils secrete?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
IL 4
The igA found in breast milk
Superficial inguinal

3. What is the pathogenesis of a candida skin test?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Delayed type hypersensitivity
Cytokine IL 10 secreted by Th2
MHC I - CD16 - CD56

4. What portion of the lymph node is not well developed in DiGeorge Syndrome?
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
...
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Paracortex

5. What is chronic mucocutaneous candidiasis d/t?
IL 4 - 5 - 10 - 6
T cell dysfunction
Acts as second signal on B cells to induce class switching to IgE and IgG
Increases expression of MHC I and MHC II and also activates NK cells

6. What lymph node drains the lateral side of the dorsum of the foot?
The igA found in breast milk
Popliteal
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
In the germinal center of secondary follicles (In the paler center)

7. What is the pathogenesis of HyperIgE syndrome? What are the labs?
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
Anti alpha subunit 3 of collagen on type IV bm
Pernicious Anemia and Hashimotos
Th cells fail to produce interferon gamma; a lot of IgE

8. Which diseases are associated with DR2?
CRP - C3b - IgM
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
delayed!
MS - hay fever - SLE - goodpastures

9. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Hemochromatosis
...
Th cells fail to produce interferon gamma; a lot of IgE

10. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
MHC II - B7
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
The igA found in breast milk
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

11. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Superior mesenteric
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
pathogenesis
A - B - C; all the D's

12. Monomer in circulation - ___ when secreted
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
encapsulated
Remove encapsulated bacateria
dimer

13. What are the autoantibodies for Mixed connective tissue disease?
Superior mesenteric
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Anti U1 RNP (ribonucleoprotein)
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

14. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
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
pale central germinal centers
False! B cell class switching requires a second signal
Cross link

15. what will NK cells do to cells covered in IgG Ab? why?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Kill them because they have CD16 on them that recognize the FcG portion
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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

16. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
except hyperacute
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

17. What is filgrastim and sargramostim? and What is it used for?
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
A j chain
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Hemochromatosis

18. The lymphocytes are ________ origin
Humoral
type four
mesenchymal
isotype

19. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IgM and IgA
Hemochromatosis
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

20. which of the hypersensitivity reactions is not Ab mediated?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Activates cytotoxic CD 8 T cells as second signal
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!
Type IV

21. 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?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
TLR ad nuclear receptors

22. What is the presentation of hyperIgM syndrome?
Sinusitis - otitis media - pneumonia
C5a
Severe pyogenic infections early in life
Anti U1 RNP (ribonucleoprotein)

23. ________ regulate the cell mediated response.
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
Humoral
Immunoflourescent staining of tissue biopsies
Lymphocytes

24. What are the major functions of Antibodies?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
not Ab mediated
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

25. What is the presentation of scid? treatment?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgAs in mothers breast milk!

26. How is the thymus organized? what happens in each section?
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
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

27. What are the three types of lymphocytes?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IgM and IgD
B - T - and NK cells
...

28. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Humoral
T cell precursor

29. What are four results of a splenectomy?
mesenchymal
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anemias (esp due to renal failure)

30. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Fab portion
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

31. What is the pathology seen in chronic transplant rejection?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Antimicrosomal and antithyroglobulin
Macrophages - Dendritic cells - B cells
Th cells fail to produce interferon gamma; a lot of IgE

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
NK cells
Paracortex; viral infection
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

33. are Th cells involved in trapping of antigens of endotoxin/LPS?
Anti mitochondrial
Sinusitis - otitis media - pneumonia
...
No because no peptide fragment!

34. Which cytokines do Th2 release and For what?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
IL 4 - 5 - 10 - 6

35. what cell surface marker is used for NK cells as it is unique to them?
Negative nitroblue tetrazolium reduction test
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
CD56
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

36. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Remove encapsulated bacateria
Its a serine protease that activates apoptosis; NK and CD8
Anti topoisomerase

37. What are the autoantibodies for systemic sclerosis?
Steroid responsive nephrotic syndrome
Sinusitis - otitis media - pneumonia
Anti topoisomerase
TLR ad nuclear receptors

38. Give three examples of bacteria that use antigenic variation and how.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Interferon gamma and IL 2

39. which B and T cell disorder presents with specifically low IgM?
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
Hereditary angioedema; PNH
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Wiskott Aldrich syndrome

40. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
All MHC 1/CD8
NK cells
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

41. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Acts as second signal on B cells to induce class switching to IgE and IgG
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
pentamer

42. What cytokines are released by Th1 cells?
Alternative splicing of mRNA
Interferon gamma and IL 2
pathogenesis
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

43. What is the pathogenesis of a hypersensitivity reaction?
Anti U1 RNP (ribonucleoprotein)
NK cells
IL 4
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

44. What are the PALS?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
MS - hay fever - SLE - goodpastures
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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

45. can igG cross the placenta?
Yes
lowest concentration
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
MS

46. What is the main cytokine released by T cells? What does it do
not Ab mediated
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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
IL 3; supports growth and differentiation of bone marrow stem cells

47. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Yes
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
T cell precursor

48. which cytokine inhibits TH2 cells? secreted by who?
acute phase reactants
Interferon gamma; Th1
T cell precursor
S. aureus - E. Coli - aspergillus

49. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
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
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

50. What are some sinopulmonary infections?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Sinusitis - otitis media - pneumonia
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)