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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 else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
IgM and IgG
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Activate macrophages
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

2. ________ regulate the cell mediated response.
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
Humoral
Immunoflourescent staining of tissue biopsies
MHC I; from RER with help of the B2 microglobulin

3. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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 :(
Receiving preformed Antibodies

4. What does IgA pick up from epithelial cells before being secreted?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Receiving preformed Antibodies
Sinusitis - otitis media - pneumonia
Secretory component

5. The Fc region is found on the...
Kill them because they have CD16 on them that recognize the FcG portion
Wiskott Aldrich syndrome
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
carboxy terminal

6. what cytokine does basophils secrete?
Sinusitis - otitis media - pneumonia
Superficial inguinal
Immunosuppression after kidney transplantation
IL 4

7. Which is the main antibody that provides passive immunity to infants?
Influenza; antigenic shift; antigenic drift
Type IV
IgG
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

8. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
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
Macrophages - Dendritic cells - B cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

9. What are the autoantibodies for wegeners granulomatosis?
Anti viral and anti tumor
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
A j chain

10. What is the treatment of acute transplant rejection?
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 :(
Glycoproteins; HLA
Cyclosporine - OKT3
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

11. Which antibody mediates immunity to worms? how?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IgE; by activating eosinophils
A - B - C; all the D's
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

12. T/F B cells do not require a second signal
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
MHC II - B7
False! B cell class switching requires a second signal
Tetanus - Botulinum - HBV - Rabies

13. Describe the complement independent Type II hypersenstivity reaction. Give an example.
No because no peptide fragment!
Superficial inguinal
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
cannot cross placenta

14. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
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!
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
Influenza; antigenic shift; antigenic drift
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

15. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Barrel hoop basement membrane fenestrations
MHC I; from RER with help of the B2 microglobulin

16. What are the autoantibodies for pemphigus bulgaris?
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
dimer
Antidesmoglein

17. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
CRP - C3b - IgM
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Interferon gamma and IL 2

18. What is the main cytokine that activates eosinophils?
IL 5
Previous transfusion; pregnant woman whose fetus had paternal antigens
IgE; by activating eosinophils
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

19. What are superantigens? give two examples.
isotype
Edema and necrosis in that region
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
Rheumatic arthritis

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

21. What is hereditary angioedema? What are the C3 levels?
MS
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
Basophils! THey want IG E class switch!
IgAs in mothers breast milk!

22. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Edema and necrosis in that region
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

23. IgM can fix complement but...
pale central germinal centers
Antimicrosomal and antithyroglobulin
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
cannot cross placenta

24. What is three common causes of severe combined immunodef? What is the result of all three?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
A - B - C; all the D's
T cell activation; no with CD 4 or CD 8
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

25. What do mature naive B lymphocytes express?
Cytokine IL 10 secreted by Th2
secondary
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IgM and IgD

26. What is the pathology of acute transplant rejection? is it reversible?
acute phase reactants
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
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

27. What are the three types of lymphocytes?
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
2 heavy chains and two light chains
B - T - and NK cells
Para aortic

28. What is anergy? why does this occur?
not Ab mediated
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IgAs in mothers breast milk!
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

29. What is the autoantibody for SLE that is nonspecific? Specific?
In the germinal center of secondary follicles (In the paler center)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IgM and IgG
Negative nitroblue tetrazolium reduction test

30. What type of fenestrations are found in the red pulp of the spleen?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Wiskott Aldrich syndrome
Barrel hoop basement membrane fenestrations
S. aureus - E. Coli - aspergillus

31. In thymic development - What is the positive selection? negative selections?
IgA
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
When you select for which MHC it will have; take out the lymphs that self react
Thrombocytopenia

32. What is an example of a parasite showing antigenic variation?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
encapsulated
Its a serine protease that activates apoptosis; NK and CD8

33. 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
Internal iliac
Anti mitochondrial
Cells that stil have weird parts of their membrane that macrophages usually bite off

34. What does granulysin do?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
MS
No because no peptide fragment!
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

35. What are the autoantibodies for sjorgens syndrome?
The patient could become cyanotic in the OR!
All MHC 1/CD8
Anti U1 RNP (ribonucleoprotein)
Anti SS- A (anti RO) and Anti SS- B

36. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
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
Lymphocytes
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
Axillary

37. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
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
isotype

38. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Paracortex
acute phase reactants
All MHC 1/CD8
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. other than mediating shock - what else does TNF alpha do? who releases it mainly?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
A chemotactic factor for neutrophils
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
Activates Th1 helper cells; Macrophages

40. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Antidote for digoxin intoxication
Hemochromatosis
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

41. What is the main function of IL 8?
Severe pyogenic infections early in life
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
Kill them because they have CD16 on them that recognize the FcG portion
A chemotactic factor for neutrophils

42. How fast does it occur?
The patient could become cyanotic in the OR!
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
All MHC 1/CD8
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

43. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
All MHC 1/CD8
Not thymus - BM

44. How do you test for type III hypersensitivity?
T cell precursor
Anti smooth muscle
Immunoflourescent staining of tissue biopsies
RNA segment reassortment

45. Name 5 ways Antibody diversity is generated?
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
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
Graves
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

46. What does CD16 on NK cells do?
Increases expression of MHC I and MHC II and also activates NK cells
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Bind FcG for antibody dependent cellular cytotoxicity
Anti topoisomerase

47. What lymph node drains the duodenum - jejunum?
Superior mesenteric
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
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

48. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Anti SS- A (anti RO) and Anti SS- B
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 the clinical use for azathioprine?
Daclizumab; prevent ACUTE rejection of renal transplant
TGF beta and IL 10
...
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)

50. which antibody activate mast cells - basophils - and eosinophils?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
opsonizes
IgE
Paracortex; viral infection