Test your basic knowledge |

USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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 a factor that is a predictor for a bad transplantation?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
dimer

2. which antibody activate mast cells - basophils - and eosinophils?
Viral neutralization of igM and IgG!
IgE
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Cyclosporine - OKT3

3. What are the autoantibodies for pemphigus bulgaris?
isotype
Para aortic
IgA
Antidesmoglein

4. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
MS - hay fever - SLE - goodpastures
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
IgM and IgD

5. What is the pathogenesis of a candida skin test?
isotype
Thrombocytopenia
Delayed type hypersensitivity
acute phase reactants

6. Which diseases are associated with DR2?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
MS - hay fever - SLE - goodpastures
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

7. when can graft versus host disease? What is the result?
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
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
Alternative splicing of mRNA
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

8. From where do cytokines come from?
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 TSh receptor
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Lymphocytes

9. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Celiac
Macrophages - Dendritic cells - B cells

10. What happens in a deficiency of C3?
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Wiskott Aldrich syndrome
secondary

11. How is i Th1 helper cell inhibited?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Cytokine IL 10 secreted by Th2

12. What does IgA pick up from epithelial cells before being secreted?
Macrophages - Dendritic cells - B cells
Paracortex
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Secretory component

13. What does interferon gamma do? What two type of cells does it attack mostly?
cannot cross placenta
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
MS - hay fever - SLE - goodpastures
A - B - C; all the D's

14. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
except hyperacute

15. T/F B cells do not require a second signal
False! B cell class switching requires a second signal
Cross link
Antibody mediated cytotoxicity; either complement dependent or complement independent
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

16. What is the presentation of Brutons agammaglobulinemia?
Activate macrophages
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Yes

17. 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)?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

18. Which disease is associated with HLA A3?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Hemochromatosis
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 3; supports growth and differentiation of bone marrow stem cells

19. what prevents NK cells from killing normal cells if their default is to kill?
Pernicious Anemia and Hashimotos
Superficial inguinal
MHC class molecules bind to KIRS or CD94 to prevent killing
In the germinal center of secondary follicles (In the paler center)

20. What is three common causes of severe combined immunodef? What is the result of all three?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
isotype
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

21. What is the main function of interferons?
MHC II - B7
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

22. Monomer in circulation - ___ when secreted
dimer
IgM and IgD
IgA
Complement activation (active in both)

23. What is the pathogenesis of acute transplant rejection? When does it occur?
Tetanus - Botulinum - HBV - Rabies
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Negative!
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

24. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
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
Negative selection
active complement pathway

25. What is the main cytokine that activates eosinophils?
Not thymus - BM
carboxy terminal
IL 5
pale central germinal centers

26. Which disease is associated with B8?
opsonizes
Graves
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Anti IF

27. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

28. What lymph node drains the breast?
IL 1 and IL 6
Axillary
Alternative splicing of mRNA
S. aureus - E. Coli - aspergillus

29. What is epo used for?
Anemias (esp due to renal failure)
Anti mitochondrial
Wiskott Aldrich syndrome
T cell activation; no with CD 4 or CD 8

30. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Activates Th1 helper cells; Macrophages
Histamine; post capillary venules - vasodilation
2 heavy chains and two light chains
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

31. What is recomb gamma interferon used for?
False! B cell class switching requires a second signal
dimer
Chronic granulomatous disease
Immunoflourescent staining of tissue biopsies

32. What is the pathogenesis of HyperIgE syndrome? What are the labs?
encapsulated
Th cells fail to produce interferon gamma; a lot of IgE
SP infections
In the germinal center of secondary follicles (In the paler center)

33. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Active; passive - fast but short half life (3 weeks!)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Lymphocytes
Anti mitochondrial

34. 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)
Severe pyogenic infections early in life
DM type I
Lymphocytes

35. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
MS - hay fever - SLE - goodpastures
IL 1 and IL 6
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

36. What does granzyme do? who secretes it?
Paracortex
Its a serine protease that activates apoptosis; NK and CD8
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
Activates cytotoxic CD 8 T cells as second signal

37. What are the autoantibodies for primary biliary cirrhosis?
T cell dysfunction
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
delayed!
Anti mitochondrial

38. Give an example of someone who could get hyperacute transplant rejection.
C5a
Previous transfusion; pregnant woman whose fetus had paternal antigens
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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

39. What are the two signals required for Th1 cells? what happens after then activated?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Not thymus - BM
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
isotype

40. What is filgrastim and sargramostim? and What is it used for?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IL 15; IL 12 - interferon Beta and interferon alpha
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

41. What is digoxin immune Fab used for?
Not thymus - BM
Activates Th1 helper cells; Macrophages
Antidote for digoxin intoxication
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

42. What is the pathology in hyperacute transplant rejection?
Rheumatic arthritis
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Activates Th1 helper cells; Macrophages

43. What lymph node drains the sigmoid colon?
Type IV
Inferior mesenteric
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

44. What does Interferon alpha and beta do? how?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Complement activation (active in both)
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

45. What does CD16 on NK cells do?
Liver! (they are proteins circulating in the blood)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Bind FcG for antibody dependent cellular cytotoxicity

46. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
RNA segment reassortment
cannot cross placenta
Rheumatic arthritis

47. Which diseases are associated with DR5?
Pernicious Anemia and Hashimotos
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Graves
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

48. describe the classic complement pathway.
Complement activation (active in both)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

49. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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

50. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
The igA found in breast milk
False! B cell class switching requires a second signal
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Daclizumab; prevent ACUTE rejection of renal transplant