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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
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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 are the autoantibodies for wegeners granulomatosis?
IL 4 - 5 - 10 - 6
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anti IF

2. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
IL 5
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Glycoproteins; HLA

3. What are the autoantibodies for sjorgens syndrome?
Negative!
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Anti SS- A (anti RO) and Anti SS- B
except hyperacute

4. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Previous transfusion; pregnant woman whose fetus had paternal antigens
Inferior mesenteric
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

5. where do NK cells develop?
Anti alpha subunit 3 of collagen on type IV bm
Not thymus - BM
...
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

6. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
secondary

7. What are four results of a splenectomy?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Antimicrosomal and antithyroglobulin
Negative selection
Cyclosporine - OKT3

8. The MALT/GALT are not...
Superficial inguinal
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
encapsulated
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

9. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Negative selection
Axillary

10. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
A chemotactic factor for neutrophils
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 :(
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

11. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Axillary
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

12. which of the hypersensitivity reactions is not Ab mediated?
Type IV
Superficial inguinal
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

13. What are the two signals required for Th1 cells? what happens after then activated?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
False! B cell class switching requires a second signal
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

14. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Local infection/inflammation; infection of the ln itself; metastasis
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

15. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Activate macrophages
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
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
Cross link

16. The secondary follicles have __________; primary follicles are dense
TGF beta and IL 10
pale central germinal centers
Stimulate the liver to release acute phase reactants
Histamine; post capillary venules - vasodilation

17. What can cause a lymph node enlargement?
Negative!
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Local infection/inflammation; infection of the ln itself; metastasis
Macrophages - Dendritic cells - B cells

18. What is colostrum?
Anti topoisomerase
Anti U1 RNP (ribonucleoprotein)
The igA found in breast milk
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

19. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
In the germinal center of secondary follicles (In the paler center)
Viral neutralization of igM and IgG!
Internal iliac

20. What are the autoantibodies for type I diabetes mellitus?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti glutamate carboxylase and anti insulin
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

21. What are the autoantibodies for graves?
IgE
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Anti TSh receptor

22. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Superficial inguinal
By transcytosis
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi

23. What is the toxicity of muromonab?
Delayed type hypersensitivity
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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

24. What is Aldesleukin? What is it used for
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
A recomb cytokine of IL 2; RCC and metastatic melanoma
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Antidote for digoxin intoxication

25. What lymph node drains the upper limb?
MHC II - B7
No because no peptide fragment!
Axillary
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

26. What is the clinical use of Muromonab?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Immunosuppression after kidney transplantation
IgE
Daclizumab; prevent ACUTE rejection of renal transplant

27. IgG...
Bind FcG for antibody dependent cellular cytotoxicity
Type IV
opsonizes
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

28. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IL 4 - 5 - 10 - 6
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

29. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Anti glutamate carboxylase and anti insulin
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

30. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Anti Jo -1
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

31. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
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!
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

32. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
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!
IgM
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
DM type I and RA

33. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
type four
Axillary
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Influenza; antigenic shift; antigenic drift

34. What are target cells?
Rheumatic arthritis
Glycoproteins; HLA
Cells that stil have weird parts of their membrane that macrophages usually bite off
Anemias (esp due to renal failure)

35. Which type of selection of thymic development provides central tolerance?
Negative selection
Pernicious Anemia and Hashimotos
...
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

36. What is muromonab - CD3 (OKT3)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Para aortic
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

37. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
T cell dysfunction
A - B - C; all the D's
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

38. What cytokines are released by Th1 cells?
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
Activate macrophages
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Interferon gamma and IL 2

39. What is the pathogenesis of HyperIgE syndrome? What are the labs?
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
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
Th cells fail to produce interferon gamma; a lot of IgE
Anti IF

40. From where do cytokines come from?
Lymphocytes
Activates Th1 helper cells; Macrophages
IL 4 - 5 - 10 - 6
Antihistone

41. Which disease is associated with HLA A3?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
pale central germinal centers
Hemochromatosis
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

42. what prevents NK cells from killing normal cells if their default is to kill?
DM type I and RA
acute phase reactants
IgM
MHC class molecules bind to KIRS or CD94 to prevent killing

43. A lymph node is a ________ lymphoid organ.
TGF beta and IL 10
secondary
IgA
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

44. Name two endogenous pyrogens
IL 1 and IL 6
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

45. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Activates Th1 helper cells; Macrophages
A j chain
RNA segment reassortment
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

46. which antibody is involved in the primary response or immediate response to an antigen?
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)
Cytokine IL 10 secreted by Th2
dimer
IgM

47. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
Anti U1 RNP (ribonucleoprotein)
MS - hay fever - SLE - goodpastures
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

48. 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?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
If there is class switching and plasma cell production (that is when memory cells are produced)

49. What is the main cytokine that activates eosinophils?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
IL 5

50. what results in symptoms of shock in an acute hemolytic transfusion reaction?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

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USMLE Step 1 Immunology

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