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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. Which is the main antibody that provides passive immunity to infants?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
IgG

2. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Acts as second signal on B cells to induce class switching to IgE and IgG
MHC I - CD16 - CD56
2 heavy chains and two light chains

3. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
delayed!
Carbohydrate
Graves

4. What lymph node drains the duodenum - jejunum?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Superior mesenteric
Increases expression of MHC I and MHC II and also activates NK cells
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

5. Which disease is associated with B8?
Graves
All MHC 1/CD8
When you select for which MHC it will have; take out the lymphs that self react
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

6. What type of fenestrations are found in the red pulp of the spleen?
secondary
Barrel hoop basement membrane fenestrations
TLR ad nuclear receptors
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

7. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Anti Ach receptor
IgE; by activating eosinophils
Rheumatic arthritis
IgG

8. What do mature naive B lymphocytes express?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
IgM and IgD
Paracortex; viral infection

9. What is immune complex disease? give an example.
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 15; IL 12 - interferon Beta and interferon alpha
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

10. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IL 3; supports growth and differentiation of bone marrow stem cells
isotype
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

11. What is the presentation of common variable immunodef? and What are the labs?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
Superficial inguinal
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

12. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Pernicious Anemia and Hashimotos

13. How is the thymus organized? what happens in each section?
MHC I - CD16 - CD56
MHC class molecules bind to KIRS or CD94 to prevent killing
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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

14. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Remove encapsulated bacateria
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

15. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Anti TSh receptor
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
TLR ad nuclear receptors

16. What is the main cytokine released by T cells? What does it do
Para aortic
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IL 3; supports growth and differentiation of bone marrow stem cells

17. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
IgE
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
dimer

18. What links the adaptive and innate immunity?
Complement activation (active in both)
IL 5
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

19. What lymph node drains the testes?
Fab portion
Para aortic
Immunosuppression after kidney transplantation
Antihistone

20. What is a type I hypersensitivity reaction? What is atopic?
mesenchymal
Yes
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Alternative splicing of mRNA

21. Which is the main antibody in the delayed or secondary response to an antigen?
Active; passive - fast but short half life (3 weeks!)
Internal iliac
IgE
IgG

22. What are superantigens? give two examples.
Interferon gamma; Th1
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
Type IV

23. The secondary follicles have __________; primary follicles are dense
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Anti mitochondrial
pale central germinal centers
Anti smooth muscle

24. What are the three types of lymphocytes?
Viral neutralization of igM and IgG!
B - T - and NK cells
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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

25. What are the cell surface proteins on NK cells?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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
MHC I - CD16 - CD56

26. Which HLA's are included in MHC I? MHC II?

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27. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
CRP - C3b - IgM
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Anti TSh receptor

28. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Axillary
The patient could become cyanotic in the OR!
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Stimulate the liver to release acute phase reactants

29. What does IL 4 do?
A - B - C; all the D's
Pernicious Anemia and Hashimotos
Acts as second signal on B cells to induce class switching to IgE and IgG
B - T - and NK cells

30. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Previous transfusion; pregnant woman whose fetus had paternal antigens
...
A j chain

31. describe the pathogenesis of delayed type IV hypersensitivity
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!
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IL 5

32. where do somatic hypermutation and class switching occur?
Anti viral and anti tumor
In the germinal center of secondary follicles (In the paler center)
Tetanus - Botulinum - HBV - Rabies
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

33. What are the autoantibodies for graves?
IgG
Anti TSh receptor
Axillary
Wiskott Aldrich syndrome

34. What does interferon gamma do? What two type of cells does it attack mostly?
encapsulated
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Anti Ach receptor
Anti alpha subunit 3 of collagen on type IV bm

35. other than eat and bite RBCs what else do Macrophages of spleen do>
Acts as second signal on B cells to induce class switching to IgE and IgG
Remove encapsulated bacateria
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
neutrophilia!

36. What is epo used for?
Anemias (esp due to renal failure)
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

37. Describe complement dependent Type II hypersensitivity. Give an example.
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti TSh receptor
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
TGF beta and IL 10

38. What are the autoantibodies for myasthenia gravis?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Anti Ach receptor
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Anti SS- A (anti RO) and Anti SS- B

39. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
IgM and IgG
IL 4
Paracortex; viral infection
IgE; by activating eosinophils

40. The ______ in the BM are DN - the DP are in the cortex of thymus
When you select for which MHC it will have; take out the lymphs that self react
Severe pyogenic infections early in life
Barrel hoop basement membrane fenestrations
T cell precursor

41. Describe the Mannose Lectin pathway
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
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
delayed!
MS

42. What are C1 - C2 - C3 - C4 important for?
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Viral neutralization of igM and IgG!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

43. What is the presentation of hyperIgM syndrome?
Internal iliac
Severe pyogenic infections early in life
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

44. What are the major functions of Antibodies?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
acute phase reactants
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

45. what prevents NK cells from killing normal cells if their default is to kill?
The igA found in breast milk
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Macrophages - Dendritic cells - B cells
MHC class molecules bind to KIRS or CD94 to prevent killing

46. What type of side chains are found on Fc region of an antibody?
secondary
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Carbohydrate

47. where are complements produced?
Secretory component
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
Liver! (they are proteins circulating in the blood)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

48. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Macrophages - Dendritic cells - B cells
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
MHC I; from RER with help of the B2 microglobulin

49. What lymph node drains the breast?
When you select for which MHC it will have; take out the lymphs that self react
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Axillary

50. What lymph node drains the upper limb?
Complement activation (active in both)
IgM and IgA
TGF beta and IL 10
Axillary