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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. What is the autoantibody for SLE that is nonspecific? Specific?
Histamine; post capillary venules - vasodilation
Antibody mediated cytotoxicity; either complement dependent or complement independent
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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

2. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
TNF alpha and IL1
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

3. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
lowest concentration
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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

4. which of the transplant rejections is antibody mediated? why does it occur?
The patient could become cyanotic in the OR!
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
lowest concentration

5. which of the hypersensitivity reactions is not Ab mediated?
Popliteal
Edema and necrosis in that region
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Type IV

6. what ensure that a memory response is generated?
Not thymus - BM
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
...
If there is class switching and plasma cell production (that is when memory cells are produced)

7. where are complements produced?
Liver! (they are proteins circulating in the blood)
IgG
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
A recomb cytokine of IL 2; RCC and metastatic melanoma

8. Describe the Mannose Lectin pathway
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Immunoflourescent staining of tissue biopsies

9. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Influenza; antigenic shift; antigenic drift
Cells that stil have weird parts of their membrane that macrophages usually bite off
Histamine; post capillary venules - vasodilation
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

10. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
Daclizumab; prevent ACUTE rejection of renal transplant
T
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 :(

11. In general What are T cells good for?
Anti viral and anti tumor
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Interferon gamma and IL 2

12. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IgE
In the germinal center of secondary follicles (In the paler center)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

13. What is a type I hypersensitivity reaction? What is atopic?
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
SP infections
DM type I
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

14. To what disease do the autoantibodies to IgG (rheumatoid factor)?
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
Rheumatic arthritis
Sinusitis - otitis media - pneumonia
Glycoproteins; HLA

15. Which helper T cells' development is induced by IL 4? IL 12?
The igA found in breast milk
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Antidesmoglein
Th2; Th1

16. What is digoxin immune Fab used for?
IL 5
IL 1 and IL 6
Antidote for digoxin intoxication
Axillary

17. ________ regulate the cell mediated response.
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti glutamate carboxylase and anti insulin
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Humoral

18. What is the cause of thymic aplasia? What is its presentation? What are the labs?
DM type I and RA
Anti smooth muscle
Influenza; antigenic shift; antigenic drift
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

19. Which disease is associated with DR3?
DM type I
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Internal iliac
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

20. What lymph node drains the lateral side of the dorsum of the foot?
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
Popliteal
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

21. What can cause a lymph node enlargement?
Active; passive - fast but short half life (3 weeks!)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
acute phase reactants
Local infection/inflammation; infection of the ln itself; metastasis

22. What cytokines to Th2 secrete?
Not thymus - BM
IL 4 - 5 - 10 - 6
Anti IF
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

23. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
IL 15; IL 12 - interferon Beta and interferon alpha
A j chain
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
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

24. What lymph node drains the rectum (above the pectinate line)?
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
Internal iliac
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

25. other than C3a - what other complement acts as an anaphyloxin?
C5a
Carbohydrate
The patient could become cyanotic in the OR!
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

26. Which disease is associated with HLA A3?
IgG
Hemochromatosis
Humoral
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

27. What happens in a deficiency of C3?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

28. What is the treatment of acute transplant rejection?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Cyclosporine - OKT3
Chronic granulomatous disease
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

29. 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?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Antibody mediated cytotoxicity; either complement dependent or complement independent

30. Complements are...
Humoral
Anti TSh receptor
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
acute phase reactants

31. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
IgM and IgG
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

32. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Popliteal
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
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)
Bind FcG for antibody dependent cellular cytotoxicity

33. which type of immunity is slow but long lasting? as opposed to...
TLR ad nuclear receptors
Active; passive - fast but short half life (3 weeks!)
A - B - C; all the D's
S. aureus - E. Coli - aspergillus

34. 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!
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
IgM and IgG
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

35. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Chronic granulomatous disease
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Activates Th1 helper cells; Macrophages

36. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
carboxy terminal
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
Glycoproteins; HLA
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia

37. Which diseases are associated with DR2?
Anti topoisomerase
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MS - hay fever - SLE - goodpastures
Yes

38. What are the autoantibodies for Mixed connective tissue disease?
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 :(
Anti U1 RNP (ribonucleoprotein)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
T

39. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
Macrophages - Dendritic cells - B cells
IgG
Daclizumab; prevent ACUTE rejection of renal transplant

40. Leukocyte adhesion defect presents with...
cannot cross placenta
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
neutrophilia!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

41. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
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
Anti Ach receptor
Its main effect is a defect in Ab opsonization for killing
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

42. How do you test for type III hypersensitivity?
IgE
Immunoflourescent staining of tissue biopsies
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

43. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
IgG
Cross link
Wiskott Aldrich syndrome
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

44. Which are the only two antiinflammatory cytokines?
Yes
delayed!
Delayed type hypersensitivity
TGF beta and IL 10

45. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
TNF alpha and IL1
IL 1 and IL 6
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Its a serine protease that activates apoptosis; NK and CD8

46. How fast does it occur?
IL 4
The patient could become cyanotic in the OR!
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
Carbohydrate

47. what mediates the type II hypersensitivity? What are the two different methods?
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule
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
Antibody mediated cytotoxicity; either complement dependent or complement independent
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

48. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Immunosuppression after kidney transplantation
Para aortic
NK cells

49. What is the most common example of passive immunity?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Local infection/inflammation; infection of the ln itself; metastasis
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IgAs in mothers breast milk!

50. What lymph node drains the upper limb?
Anti mitochondrial
No because no peptide fragment!
Receiving preformed Antibodies
Axillary