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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 bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Lymphocytes
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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

2. what will NK cells do to cells covered in IgG Ab? why?
Kill them because they have CD16 on them that recognize the FcG portion
Receiving preformed Antibodies
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

3. How does igA cross the epithelium?
Daclizumab; prevent ACUTE rejection of renal transplant
By transcytosis
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

4. Which antibodies can be multimeric?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Receiving preformed Antibodies
IgE; by activating eosinophils
IgM and IgA

5. What are the autoantibodies for Celiac disease?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

6. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Anti smooth muscle
...
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Wiskott Aldrich syndrome

7. Name two endogenous pyrogens
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
IL 1 and IL 6
T cell precursor
No because no peptide fragment!

8. What is the clinical use of Muromonab?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
Immunosuppression after kidney transplantation

9. what secretes IL 4?
Basophils! THey want IG E class switch!
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
Glycoproteins; HLA
Anti viral and anti tumor

10. what prevents NK cells from killing normal cells if their default is to kill?
TNF alpha and IL1
B - T - and NK cells
MHC class molecules bind to KIRS or CD94 to prevent killing
Wiskott Aldrich syndrome

11. What are the autoantibodies for type I diabetes mellitus?
DM type I and RA
Anti glutamate carboxylase and anti insulin
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
A recomb cytokine of IL 2; RCC and metastatic melanoma

12. What does CD16 on NK cells do?
pale central germinal centers
Bind FcG for antibody dependent cellular cytotoxicity
Hemochromatosis
Remove encapsulated bacateria

13. What are the autoantibodies for systemic sclerosis?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anti topoisomerase
Liver! (they are proteins circulating in the blood)
Fc

14. What are the labs in brutons agammaglobulinemia?
Cross link
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Celiac

15. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Cross link
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
neutrophilia!
Alternative splicing of mRNA

16. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Fab portion
Cells that stil have weird parts of their membrane that macrophages usually bite off
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

17. what mediates the type II hypersensitivity? What are the two different methods?
Antibody mediated cytotoxicity; either complement dependent or complement independent
cannot cross placenta
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Antihistone

18. What is the cause of thymic aplasia? What is its presentation? What are the labs?
IgM and IgD
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
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
TNF alpha and IL1

19. How is the thymus organized? what happens in each section?
Cytokine IL 10 secreted by Th2
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
not Ab mediated
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

20. Describe the Mannose Lectin pathway
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
Previous transfusion; pregnant woman whose fetus had paternal antigens

21. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Anti U1 RNP (ribonucleoprotein)
Negative nitroblue tetrazolium reduction test
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Glycoproteins; HLA

22. What is the most common selective Ig deficiency? What is the presentation?
RNA segment reassortment
dimer
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Glycoproteins; HLA

23. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Superficial inguinal
TNF alpha and IL1
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

24. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Anti viral and anti tumor
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Histamine; post capillary venules - vasodilation

25. What is colostrum?
IL 3; supports growth and differentiation of bone marrow stem cells
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
Interferon gamma; Th1
The igA found in breast milk

26. What is passive immunity?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Receiving preformed Antibodies
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!
Negative!

27. What lymph node drains the breast?
C5a
Antidote for digoxin intoxication
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 :(
Axillary

28. What are the main Cell surface proteins on T cells?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
...
Stimulate the liver to release acute phase reactants

29. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Anti mitochondrial
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

30. IgM can fix complement but...
cannot cross placenta
Severe pyogenic infections early in life
Chronic granulomatous disease
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

31. Which is the most abundant antibody in blood?
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IgG
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

32. What cytokines to Th2 secrete?
...
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
IL 4 - 5 - 10 - 6

33. What is the presentation of hyperIgM syndrome?
T cell activation; no with CD 4 or CD 8
CD56
Severe pyogenic infections early in life
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

34. What are the three types of lymphocytes?
active complement pathway
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
B - T - and NK cells

35. How fast does it occur?
The patient could become cyanotic in the OR!
Type IV
Celiac
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

36. What are some sinopulmonary infections?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Sinusitis - otitis media - pneumonia
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgG

37. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Pernicious Anemia and Hashimotos

38. What is the receptor for EBV? On what cells is that located?
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Histamine; post capillary venules - vasodilation

39. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Rheumatic arthritis
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Histamine; post capillary venules - vasodilation
Activate macrophages

40. 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?
Anti viral and anti tumor
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
T cell activation; no with CD 4 or CD 8

41. Which type of selection of thymic development provides central tolerance?
IgE
Negative selection
Immunosuppression after kidney transplantation
TGF beta and IL 10

42. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Superficial inguinal
Paracortex; viral infection
Inferior mesenteric

43. What is the clinical use for azathioprine?
Anemias (esp due to renal failure)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
...
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

44. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
Axillary
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

45. How is the antigen loaded onto a MHC II?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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

46. How is sirolimus different from tacrolimus?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
A recomb cytokine of IL 2; RCC and metastatic melanoma
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

47. What is the main function of IL 12? other than macrophages who else can release IL 12?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

48. What is the presentation of scid? treatment?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
MHC II - B7
Wiskott Aldrich syndrome
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!

49. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
All MHC 1/CD8
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

50. What do multimeric antibodies require for assembly?
NK cells
A j chain
Axillary
opsonizes