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. Type IV hypersensitivity is i...
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
not Ab mediated
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

2. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
pathogenesis
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

3. other than mediating shock - what else does TNF alpha do? who releases it mainly?
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
IgA
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Activates Th1 helper cells; Macrophages

4. What are the autoantibodies for drug induced lupus?
IgM and IgA
Antihistone
IgG
Carbohydrate

5. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
T
Anti glutamate carboxylase and anti insulin
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
TNF alpha and IL1

6. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
encapsulated
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

7. What is three common causes of severe combined immunodef? What is the result of all three?
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
IgM and IgG
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

8. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
If there is class switching and plasma cell production (that is when memory cells are produced)
dimer
...
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

9. What does IL 4 do?
Liver! (they are proteins circulating in the blood)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Acts as second signal on B cells to induce class switching to IgE and IgG
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

10. What links the adaptive and innate immunity?
IL 5
Complement activation (active in both)
SP infections
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

11. what mediates the type II hypersensitivity? What are the two different methods?
Tetanus - Botulinum - HBV - Rabies
Antibody mediated cytotoxicity; either complement dependent or complement independent
MS
Anti topoisomerase

12. What is the clinical use of Muromonab?
IgG
Negative!
Immunosuppression after kidney transplantation
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

13. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IL 4 - 5 - 10 - 6
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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

14. A lymph node is a ________ lymphoid organ.
Glycoproteins; HLA
secondary
Popliteal
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

15. What are the autoantibodies for graves?
Antimicrosomal and antithyroglobulin
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!
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti TSh receptor

16. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Activate macrophages
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

17. What are the two signals to kill for NK cells?
Steroid responsive nephrotic syndrome
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Type IV

18. What are the autoantibodies for Celiac disease?
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgG

19. give an example of how influenza does a major antigenic shift.
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
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
RNA segment reassortment
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

20. What are the cell surface proteins on NK cells?
IgG
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Recom IL 11; thrombocytopenia
MHC I - CD16 - CD56

21. __________ are a part of the innate system.
Antidote for digoxin intoxication
NK cells
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Popliteal

22. What is thrombopoietin used for?
MHC I; from RER with help of the B2 microglobulin
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Thrombocytopenia
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

23. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
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
neutrophilia!
TGF beta and IL 10

24. What are the three types of APCs?
Macrophages - Dendritic cells - B cells
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
TNF alpha and IL1
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

25. To what portion of the Antibody do the complements bind?
DM type I
MS
carboxy terminal
Fc

26. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
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
...
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Anti glutamate carboxylase and anti insulin

27. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Histamine; post capillary venules - vasodilation
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

28. Which cytokines do Th2 release and For what?
IgE; by activating 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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Antidote for digoxin intoxication

29. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
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
Rheumatic arthritis
Its main effect is a defect in Ab opsonization for killing

30. The secondary follicles have __________; primary follicles are dense
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
pale central germinal centers
Anti smooth muscle
Anti viral and anti tumor

31. where do somatic hypermutation and class switching occur?
2 heavy chains and two light chains
Axillary
In the germinal center of secondary follicles (In the paler center)
neutrophilia!

32. What can cause a lymph node enlargement?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Local infection/inflammation; infection of the ln itself; metastasis
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

33. What are the labs in brutons agammaglobulinemia?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

34. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
T cell precursor

35. What is a factor that is a predictor for a bad transplantation?
When you select for which MHC it will have; take out the lymphs that self react
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Secretory component
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

36. What are target cells?
Cells that stil have weird parts of their membrane that macrophages usually bite off
TLR ad nuclear receptors
SP infections
Th2; Th1

37. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

38. What lymph node drains the duodenum - jejunum?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Superior mesenteric
Secretory component

39. Which helper T cells' development is induced by IL 4? IL 12?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Th2; Th1
Basophils! THey want IG E class switch!
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

40. What does IgA pick up from epithelial cells before being secreted?
Secretory component
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
T cell activation; no with CD 4 or CD 8

41. Which MHC presents intracellular peptides? how so?
T cell activation; no with CD 4 or CD 8
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
MHC I; from RER with help of the B2 microglobulin
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

42. What do multimeric antibodies require for assembly?
IL 1 and IL 6
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
A j chain

43. What is epo used for?
Anemias (esp due to renal failure)
Delayed type hypersensitivity
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
A chemotactic factor for neutrophils

44. Which is the main antibody that provides passive immunity to infants?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

45. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Anti glutamate carboxylase and anti insulin
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

46. How is i Th1 helper cell inhibited?
Anti alpha subunit 3 of collagen on type IV bm
Cytokine IL 10 secreted by Th2
active complement pathway
Activates Th1 helper cells; Macrophages

47. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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

48. What is the main function of IL 12? other than macrophages who else can release IL 12?
TLR ad nuclear receptors
acute phase reactants
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

49. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
IgM and IgD
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
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

50. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii