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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?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
Activate macrophages

2. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
MS
Fab portion
Increases expression of MHC I and MHC II and also activates NK cells

3. What is the clinical use for azathioprine?
...
IgM and IgD
Th2; Th1
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

4. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Anti alpha subunit 3 of collagen on type IV bm
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
DM type I and RA

5. which B and T cell disorder presents with specifically low IgM?
type four
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
Wiskott Aldrich syndrome

6. What is a factor that is a predictor for a bad transplantation?
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
Anemias (esp due to renal failure)
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

7. Name 5 ways Antibody diversity is generated?
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
IgA
Local infection/inflammation; infection of the ln itself; metastasis
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

8. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
Anti TSh receptor
Barrel hoop basement membrane fenestrations
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

9. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Anti Ach receptor
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

10. is IgM an opsonizer?
A chemotactic factor for neutrophils
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Negative!
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

11. 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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Acts as second signal on B cells to induce class switching to IgE and IgG
DM type I and RA

12. What does it mean if there are igM in the serum at birth?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
carboxy terminal

13. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
IgM
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
opsonizes
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

14. IgM can fix complement but...
cannot cross placenta
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Delayed type hypersensitivity

15. What is epo used for?
Activates Th1 helper cells; Macrophages
Anemias (esp due to renal failure)
IL 1 and IL 6
Secretory component

16. How is the antigen loaded onto a MHC II?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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. where are complements produced?
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
Increases expression of MHC I and MHC II and also activates NK cells
IL 4
Liver! (they are proteins circulating in the blood)

18. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
By transcytosis
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
Activate macrophages
MS - hay fever - SLE - goodpastures

19. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IL 1 and IL 6
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Superficial inguinal

20. What portion of the lymph node is not well developed in DiGeorge Syndrome?
DM type I
Wiskott Aldrich syndrome
Paracortex
Anti smooth muscle

21. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IL 3; supports growth and differentiation of bone marrow stem cells
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IgA

22. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
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
Superficial inguinal

23. What type of side chains are found on Fc region of an antibody?
Inferior mesenteric
except hyperacute
Carbohydrate
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

24. Which MHC presents intracellular peptides? how so?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
MHC I; from RER with help of the B2 microglobulin
Local infection/inflammation; infection of the ln itself; metastasis
Anti SS- A (anti RO) and Anti SS- B

25. Which disease is associated with B8?
Anti topoisomerase
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Graves
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

26. Leukocyte adhesion defect presents with...
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
neutrophilia!
IgA
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

27. What is the defect in hyper IgM syndrome? What are the lab results?
Complement activation (active in both)
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
Antibody mediated cytotoxicity; either complement dependent or complement independent

28. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Fab portion
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

29. give an example of how influenza does a major antigenic shift.
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
RNA segment reassortment
CD56
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

30. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Superficial inguinal
Hereditary angioedema; PNH

31. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
Histamine; post capillary venules - vasodilation
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
Its a serine protease that activates apoptosis; NK and CD8

32. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
Internal iliac
Influenza; antigenic shift; antigenic drift
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

33. What is the most common example of passive immunity?
neutrophilia!
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Graves
IgAs in mothers breast milk!

34. what cell surface marker is used for NK cells as it is unique to them?
IgG
CD56
Pernicious Anemia and Hashimotos
CRP - C3b - IgM

35. what ensure that a memory response is generated?
Negative!
If there is class switching and plasma cell production (that is when memory cells are produced)
lowest concentration
Steroid responsive nephrotic syndrome

36. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
CRP - C3b - IgM
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

37. what mediates the type II hypersensitivity? What are the two different methods?
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
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
Antibody mediated cytotoxicity; either complement dependent or complement independent
Cyclosporine - OKT3

38. What are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Activates Th1 helper cells; Macrophages
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

39. What does interferon gamma do to be antiviral?
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
IgM and IgG
Increases expression of MHC I and MHC II and also activates NK cells
opsonizes

40. Name two endogenous pyrogens
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IL 1 and IL 6
IgAs in mothers breast milk!
Superficial inguinal

41. What are the two signals required for Th1 cells? what happens after then activated?
Activates cytotoxic CD 8 T cells as second signal
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the

42. What is the main function of interferons?
Activates Th1 helper cells; Macrophages
Superficial inguinal
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
pale central germinal centers

43. The Fc region is found on the...
Cross link
carboxy terminal
opsonizes
Histamine; post capillary venules - vasodilation

44. What is the main cytokine that activates eosinophils?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Pernicious Anemia and Hashimotos
A chemotactic factor for neutrophils
IL 5

45. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
encapsulated

46. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
T cell activation; no with CD 4 or CD 8

47. What are the main symptoms of T cell immunodeficiencies?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

48. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Hereditary angioedema; PNH
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 and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Not thymus - BM

49. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Th2; Th1
except hyperacute
A chemotactic factor for neutrophils

50. which antibodies prevent antigens from binding mucosal surfaces?
Superficial inguinal
IgA
NK cells
Anti smooth muscle