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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.
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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 is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
IL 4 - 5 - 10 - 6
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
mesenchymal
IgA

2. What does it mean if there are igM in the serum at birth?
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

3. What are MHC's necessary for? By themselves?
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
T cell activation; no with CD 4 or CD 8
Basophils! THey want IG E class switch!

4. Name 5 ways Antibody diversity is generated?
No because no peptide fragment!
Histamine; post capillary venules - vasodilation
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

5. which B and T cell disorder presents with specifically low IgM?
heavy chains
Wiskott Aldrich syndrome
The patient could become cyanotic in the OR!
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

6. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
DM type I
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
Carbohydrate

7. What lymph node drains the sigmoid colon?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Inferior mesenteric
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

8. From where do cytokines come from?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
pathogenesis
MHC II - B7
Lymphocytes

9. is IgM an opsonizer?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Negative!
Hemochromatosis
Yes

10. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Superior mesenteric
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

11. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Superficial inguinal
Influenza; antigenic shift; antigenic drift
IgM
Anti mitochondrial

12. Give an example of someone who could get hyperacute transplant rejection.
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Viral neutralization of igM and IgG!
Previous transfusion; pregnant woman whose fetus had paternal antigens

13. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
By transcytosis
Superficial inguinal
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

14. Which MHC presents intracellular peptides? how so?
pale central germinal centers
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Increases expression of MHC I and MHC II and also activates NK cells
MHC I; from RER with help of the B2 microglobulin

15. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
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
Antidote for digoxin intoxication
Activates Th1 helper cells; Macrophages

16. Which type of selection of thymic development provides central tolerance?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
NK cells

17. What are the autoantibodies for polymyositis and dermatomyositis?
Anti Jo -1
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
Anti IF
MHC I - CD16 - CD56

18. The MALT/GALT are not...
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
encapsulated
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

19. What is the mechanism for sirolimus? what else it known as?
Not thymus - BM
type four
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
pale central germinal centers

20. Which diseases are associated with DR5?
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
Pernicious Anemia and Hashimotos
Not thymus - BM
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

21. what results in symptoms of shock in an acute hemolytic transfusion reaction?
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
The patient could become cyanotic in the OR!
Glycoproteins; HLA

22. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Fab portion
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!
MS - hay fever - SLE - goodpastures
Rheumatic arthritis

23. Which antibodies can be multimeric?
IgM and IgA
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IL 4 - 5 - 10 - 6

24. A lymph node is a ________ lymphoid organ.
secondary
Cyclosporine - OKT3
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
C5a

25. What links the adaptive and innate immunity?
Complement activation (active in both)
IL 1 and IL 6
IgG
Delayed type hypersensitivity

26. What are the three types of lymphocytes?
Anti viral and anti tumor
B - T - and NK cells
DM type I and RA
Active; passive - fast but short half life (3 weeks!)

27. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
The igA found in breast milk
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

28. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
except hyperacute
Th2; Th1
heavy chains

29. Which disease is associated with HLA A3?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Hemochromatosis
Type IV
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

30. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
isotype

31. what characterizes an arthus reaction?
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!
Edema and necrosis in that region
Negative nitroblue tetrazolium reduction test
IgG

32. What is the treatment of acute transplant rejection?
...
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Cyclosporine - OKT3

33. What lymph node drains the anal canal (below the pectinate line)?
Pernicious Anemia and Hashimotos
Superficial inguinal
heavy chains
Wiskott Aldrich syndrome

34. What is immune complex disease? give an example.
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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

35. What is the main cytokine that activates eosinophils?
Anti Ach receptor
Tetanus - Botulinum - HBV - Rabies
Cells that stil have weird parts of their membrane that macrophages usually bite off
IL 5

36. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
IgG
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Histamine; post capillary venules - vasodilation

37. which type of immunity is slow but long lasting? as opposed to...
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
cannot cross placenta
SP infections
Active; passive - fast but short half life (3 weeks!)

38. what mediates the type II hypersensitivity? What are the two different methods?
Th2; Th1
Antibody mediated cytotoxicity; either complement dependent or complement independent
Pernicious Anemia and Hashimotos
MS

39. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Bind FcG for antibody dependent cellular cytotoxicity
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
TNF alpha and IL1
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

40. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Steroid responsive nephrotic syndrome
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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

41. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
By transcytosis
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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

42. The lymphocytes are ________ origin
mesenchymal
Anti IF
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
CD56

43. which antibodies prevent antigens from binding mucosal surfaces?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
C5a
IgA
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

44. What are the main symptoms of T cell immunodeficiencies?
Its main effect is a defect in Ab opsonization for killing
pale central germinal centers
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

45. What lymph node drains the scrotum?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Interferon gamma; Th1
Superficial inguinal
By transcytosis

46. What is the main function of IL 8?
Anti U1 RNP (ribonucleoprotein)
Stimulate the liver to release acute phase reactants
A chemotactic factor for neutrophils
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

47. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
TGF beta and IL 10
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

48. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
T cell precursor
IgA
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 4 - 5 - 10 - 6

49. which cytokine inhibits TH2 cells? secreted by who?
Interferon gamma; Th1
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
A chemotactic factor for neutrophils
pentamer

50. which antibody activate mast cells - basophils - and eosinophils?
Antimicrosomal and antithyroglobulin
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
IgE
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)