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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 disease is associated with DR7?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
IgM
Steroid responsive nephrotic syndrome

2. What do multimeric antibodies require for assembly?
A j chain
IgG
IL 3; supports growth and differentiation of bone marrow stem cells
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

3. What is three common causes of severe combined immunodef? What is the result of all three?
No because no peptide fragment!
In the germinal center of secondary follicles (In the paler center)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

4. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
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
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
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
heavy chains

5. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
Celiac
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
Its a serine protease that activates apoptosis; NK and CD8

6. What lymph node drains the sigmoid colon?
Glycoproteins; HLA
Local infection/inflammation; infection of the ln itself; metastasis
Inferior mesenteric
A recomb cytokine of IL 2; RCC and metastatic melanoma

7. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Anti IF
Fc
Influenza; antigenic shift; antigenic drift
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

8. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
IgM
Antimicrosomal and antithyroglobulin
except hyperacute
Lymphocytes

9. which cytokine inhibits TH2 cells? secreted by who?
Anemias (esp due to renal failure)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Interferon gamma; Th1
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

10. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
MS
Negative nitroblue tetrazolium reduction test
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

11. What are the autoantibodies for Celiac disease?
Paracortex
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

12. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Antidote for digoxin intoxication
MHC II - B7
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

13. What is colostrum?
isotype
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
The igA found in breast milk
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

14. Leukocyte adhesion defect presents with...
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
Axillary
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
neutrophilia!

15. What is the clinical use of Muromonab?
Superior mesenteric
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Not thymus - BM
Immunosuppression after kidney transplantation

16. can igG cross the placenta?
Yes
Fab portion
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

17. What does interferon gamma do? What two type of cells does it attack mostly?
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
heavy chains
pentamer

18. describe the pathogenesis of delayed type IV hypersensitivity
Remove encapsulated bacateria
T cell precursor
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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

19. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Anti topoisomerase

20. What does IL 4 do?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
A chemotactic factor for neutrophils
Acts as second signal on B cells to induce class switching to IgE and IgG
Complement activation (active in both)

21. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Activate macrophages
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Glycoproteins; HLA

22. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Type IV
pentamer
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

23. Which diseases are associated with DR4?
Local infection/inflammation; infection of the ln itself; metastasis
DM type I and RA
IgM and IgG
Anemias (esp due to renal failure)

24. what secretes IL 4?
Receiving preformed Antibodies
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Basophils! THey want IG E class switch!
Axillary

25. What are the autoantibodies for other vasculitides?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
CRP - C3b - IgM
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

26. which of the hypersensitivity reactions is not Ab mediated?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Type IV

27. What is filgrastim and sargramostim? and What is it used for?
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

28. What are the autoantibodies for goodpastures syndrome?
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Rheumatic arthritis
Anti alpha subunit 3 of collagen on type IV bm

29. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
IgM
Its main effect is a defect in Ab opsonization for killing
Recom IL 11; thrombocytopenia
2 heavy chains and two light chains

30. __________ are a part of the innate system.
NK cells
Its a serine protease that activates apoptosis; NK and CD8
Secretory component
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

31. What is the main cytokine that activates eosinophils?
lowest concentration
Anti alpha subunit 3 of collagen on type IV bm
IL 5
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

32. What is the pathogenesis of a hypersensitivity reaction?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Steroid responsive nephrotic syndrome
T cell activation; no with CD 4 or CD 8
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

33. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
CRP - C3b - IgM
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

34. 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!)
Anti alpha subunit 3 of collagen on type IV bm
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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

35. Which disease is associated with HLA A3?
MHC II - B7
Activate macrophages
Hemochromatosis
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

36. What do mature naive B lymphocytes express?
Daclizumab; prevent ACUTE rejection of renal transplant
Bind FcG for antibody dependent cellular cytotoxicity
IgM and IgD
Steroid responsive nephrotic syndrome

37. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

38. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Negative nitroblue tetrazolium reduction test
Its main effect is a defect in Ab opsonization for killing
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
...

39. What does granulysin do?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Th2; Th1
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

40. what cytokine does basophils secrete?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Alternative splicing of mRNA
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
IL 4

41. What are the major functions of Antibodies?
heavy chains
pale central germinal centers
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Glycoproteins; HLA

42. What is the most common selective Ig deficiency? What is the presentation?
...
Immunoflourescent staining of tissue biopsies
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

43. Which antibodies can be multimeric?
IgM and IgA
Immunosuppression after kidney transplantation
Its main effect is a defect in Ab opsonization for killing
A chemotactic factor for neutrophils

44. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
NK cells
T
Superficial inguinal

45. What lymph node drains the testes?
Para aortic
IgE; by activating eosinophils
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Wiskott Aldrich syndrome

46. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
IgAs in mothers breast milk!

47. What are the autoantibodies for type I diabetes mellitus?
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti glutamate carboxylase and anti insulin
Popliteal

48. What is immune complex disease? give an example.
CRP - C3b - IgM
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Glycoproteins; HLA
Paracortex

49. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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
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)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Immunosuppression after kidney transplantation

50. How fast does it occur?
Interferon gamma and IL 2
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Liver! (they are proteins circulating in the blood)
The patient could become cyanotic in the OR!