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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 are the autoantibodies for Celiac disease?
Viral neutralization of igM and IgG!
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Type IV
Para aortic

2. What is the common variable immunodeficiency ? How is it different from Brutons?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
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

3. Which diseases are associated with DR4?
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
DM type I and RA
Anti IF
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

4. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Cytokine IL 10 secreted by Th2

5. IgE has the ___________ in the serum
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
Paracortex
lowest concentration
Acts as second signal on B cells to induce class switching to IgE and IgG

6. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
Anti IF
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

7. What is the clinical use for azathioprine?
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
...
IgM and IgA
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

8. which of the transplant rejections is antibody mediated? why does it occur?
A - B - C; all the D's
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Para aortic
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d

9. Describe the Mannose Lectin pathway
Type IV
Cells that stil have weird parts of their membrane that macrophages usually bite off
Its main effect is a defect in Ab opsonization for killing
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

10. Type IV hypersensitivity is i...
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)
IgM and IgG
not Ab mediated
Acts as second signal on B cells to induce class switching to IgE and IgG

11. What is thrombopoietin used for?
IL 1 and IL 6
Superficial inguinal
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Thrombocytopenia

12. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Anti alpha subunit 3 of collagen on type IV bm
CRP - C3b - IgM
Hemochromatosis

13. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
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
heavy chains
The patient could become cyanotic in the OR!

14. What is the main cytokine that activates eosinophils?
Wiskott Aldrich syndrome
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Negative!
IL 5

15. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Superficial inguinal
Barrel hoop basement membrane fenestrations
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
secondary

16. What links the adaptive and innate immunity?
Anti glutamate carboxylase and anti insulin
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Complement activation (active in both)

17. What is the autoantibody for SLE that is nonspecific? Specific?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IgM and IgD
DM type I and RA
IL 15; IL 12 - interferon Beta and interferon alpha

18. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
Activates cytotoxic CD 8 T cells as second signal
Carbohydrate
Complement activation (active in both)

19. Which antibodies can be multimeric?
IgM and IgA
Macrophages - Dendritic cells - B cells
CRP - C3b - IgM
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

20. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
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
T cell dysfunction

21. 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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
SP infections

22. can igG cross the placenta?
Yes
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
False! B cell class switching requires a second signal

23. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
B - T - and NK cells
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Axillary
DM type I

24. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Superficial inguinal
...
Histamine; post capillary venules - vasodilation

25. How does igA cross the epithelium?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Negative nitroblue tetrazolium reduction test
By transcytosis

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

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27. What is the pathogenesis of acute transplant rejection? When does it occur?
Viral neutralization of igM and IgG!
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

28. which antibodies prevent antigens from binding mucosal surfaces?
IgA
Humoral
secondary
Anti SS- A (anti RO) and Anti SS- B

29. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
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 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
pale central germinal centers

30. Which diseases are associated with DR5?
Anti alpha subunit 3 of collagen on type IV bm
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Pernicious Anemia and Hashimotos
Paracortex

31. What are the autoantibodies for primary biliary cirrhosis?
...
Anti mitochondrial
Cytokine IL 10 secreted by Th2
Anti topoisomerase

32. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
DM type I
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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

33. Give an example of someone who could get hyperacute transplant rejection.
Th cells fail to produce interferon gamma; a lot of IgE
...
Axillary
Previous transfusion; pregnant woman whose fetus had paternal antigens

34. What are the main cell surface proteins on B cells?
Its a serine protease that activates apoptosis; NK and CD8
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anti Ach receptor
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

35. What are the major functions of Antibodies?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Daclizumab; prevent ACUTE rejection of renal transplant
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

36. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
When you select for which MHC it will have; take out the lymphs that self react
RNA segment reassortment

37. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
neutrophilia!
active complement pathway
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

38. What is the marginal zone of the spleen? what happens there?
All MHC 1/CD8
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
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
IL 4

39. which type of immunity is slow but long lasting? as opposed to...
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Negative nitroblue tetrazolium reduction test
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Active; passive - fast but short half life (3 weeks!)

40. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Immunoflourescent staining of tissue biopsies
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
Anti IF
...

41. Which is the most abundant antibody in blood?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IgG
pathogenesis

42. What is a factor that is a predictor for a bad transplantation?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
cannot cross placenta
Superficial inguinal

43. What cytokines to Th2 secrete?
Anti alpha subunit 3 of collagen on type IV bm
Anti U1 RNP (ribonucleoprotein)
IL 4 - 5 - 10 - 6
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

44. what happens in a deficiency of C1 esterase inhibitor? DAF?
Hereditary angioedema; PNH
opsonizes
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
Severe pyogenic infections early in life

45. What does it mean if there are igM in the serum at birth?
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

46. The two heavy chains of an antibody contribute to the...
Antibody mediated cytotoxicity; either complement dependent or complement independent
Fab portion
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Cells that stil have weird parts of their membrane that macrophages usually bite off

47. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IgG
isotype
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

48. in which immunodef order do you see a lot of pus? no pus?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Activates cytotoxic CD 8 T cells as second signal

49. What is the late phase reaction of anaphylaxis allergy? what mediates it?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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)
Anti alpha subunit 3 of collagen on type IV bm

50. From where do cytokines come from?
Superficial inguinal
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Thrombocytopenia
Lymphocytes