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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. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
The igA found in breast milk
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

2. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
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
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

3. IgE has the ___________ in the serum
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
lowest concentration
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
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

4. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
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!
Anti Jo -1
RNA segment reassortment
Anti topoisomerase

5. Which disease is associated with HLA A3?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Hemochromatosis
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

6. What does interferon gamma do? What two type of cells does it attack mostly?
Its main effect is a defect in Ab opsonization for killing
Negative!
Alternative splicing of mRNA
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

7. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

8. What is the main function of IL 12? other than macrophages who else can release IL 12?
...
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

9. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
Inferior mesenteric
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
...

10. What are the T cell functions?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
...
heavy chains
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

11. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Cyclosporine - OKT3
Acts as second signal on B cells to induce class switching to IgE and IgG

12. What is a type I hypersensitivity reaction? What is atopic?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
MHC I - CD16 - CD56
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IgA

13. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Anti topoisomerase
Type IV
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

14. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Stimulate the liver to release acute phase reactants
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

15. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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

16. what mediates the type II hypersensitivity? What are the two different methods?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
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

17. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

18. Which type of selection of thymic development provides central tolerance?
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 :(
C5a
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Negative selection

19. which of the transplant rejections is antibody mediated? why does it occur?
Glycoproteins; HLA
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Receiving preformed Antibodies
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

20. 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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti Jo -1
Superior mesenteric

21. What is the main function of interferons?
Popliteal
False! B cell class switching requires a second signal
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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

22. which cytokine inhibits TH2 cells? secreted by who?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Interferon gamma; Th1
Antidesmoglein
Thrombocytopenia

23. Which disease is associated with DR3?
DM type I
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
T cell precursor
IgM and IgD

24. What is the main cytokine that activates eosinophils?
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
IL 5
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Active; passive - fast but short half life (3 weeks!)

25. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Pernicious Anemia and Hashimotos
By transcytosis
TNF alpha and IL1
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

26. Which diseases are associated with DR2?
Anti smooth muscle
MS - hay fever - SLE - goodpastures
secondary
Severe pyogenic infections early in life

27. Name the three opsonins
Antidesmoglein
The patient could become cyanotic in the OR!
CRP - C3b - IgM
TGF beta and IL 10

28. How does the alternative pathway lead to MAC activation?
Anti U1 RNP (ribonucleoprotein)
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
...
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

29. describe the pathogenesis of delayed type IV hypersensitivity
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Lymphocytes
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Th2; Th1

30. 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)
DM type I and RA
Activate macrophages
Internal iliac

31. IgG...
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
opsonizes
Secretory component
mesenchymal

32. What is three common causes of severe combined immunodef? What is the result of all three?
Carbohydrate
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IL 15; IL 12 - interferon Beta and interferon alpha

33. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
Graves
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

34. 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?
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
Antidote for digoxin intoxication
Tetanus - Botulinum - HBV - Rabies
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

35. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Stimulate the liver to release acute phase reactants
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Daclizumab; prevent ACUTE rejection of renal transplant

36. What happens in a deficiency of C3?
T cell dysfunction
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Cross link
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

37. Describe complement dependent Type II hypersensitivity. Give an example.
A - B - C; all the D's
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
Anti viral and anti tumor
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

38. Which diseases are associated with DR4?
DM type I and RA
Steroid responsive nephrotic syndrome
encapsulated
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

39. What cytokines are released by Th1 cells?
Axillary
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Interferon gamma and IL 2
Viral neutralization of igM and IgG!

40. __________ are a part of the innate system.
Superficial inguinal
No because no peptide fragment!
NK 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

41. What bugs can actually infect the lymph node itself?
MS - hay fever - SLE - goodpastures
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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

42. What is the clinical use for azathioprine?
Antidote for digoxin intoxication
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
...
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

43. Which antibodies can be multimeric?
Cells that stil have weird parts of their membrane that macrophages usually bite off
opsonizes
Activates cytotoxic CD 8 T cells as second signal
IgM and IgA

44. What are the main symptoms of B cell immunodeficiencies?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
SP infections

45. What are the autoantibodies for pemphigus bulgaris?
Antidote for digoxin intoxication
Antidesmoglein
IL 15; IL 12 - interferon Beta and interferon alpha
IgG

46. What is oprelevkin? and What is it used for?
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
In the germinal center of secondary follicles (In the paler center)
Anti alpha subunit 3 of collagen on type IV bm
Recom IL 11; thrombocytopenia

47. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Severe pyogenic infections early in life
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

48. What is an example of a parasite showing antigenic variation?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

49. What are the mediators that mast cells release?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti TSh receptor
Th cells fail to produce interferon gamma; a lot of IgE
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

50. What are MHC's necessary for? By themselves?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Immunosuppression after kidney transplantation
T cell activation; no with CD 4 or CD 8