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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. in which immunodef order do you see a lot of pus? no pus?
S. aureus - E. Coli - aspergillus
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Anti mitochondrial

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

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3. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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
Antihistone
Negative!
Humoral

4. What is the most common example of passive immunity?
IgAs in mothers breast milk!
T cell activation; no with CD 4 or CD 8
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

5. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Antimicrosomal and antithyroglobulin
MHC I; from RER with help of the B2 microglobulin
Receiving preformed Antibodies

6. IgM can exist as a _______ also
secondary
acute phase reactants
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
pentamer

7. What are the PALS?
Chronic granulomatous disease
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Antidesmoglein
MHC II - B7

8. What does granulysin do?
DM type I
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Tetanus - Botulinum - HBV - Rabies
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

9. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
not Ab mediated
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

10. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IL 15; IL 12 - interferon Beta and interferon alpha

11. What lymph node drains the breast?
Stimulate the liver to release acute phase reactants
Axillary
Acts as second signal on B cells to induce class switching to IgE and IgG
Thrombocytopenia

12. What is colostrum?
Anti TSh receptor
Kill them because they have CD16 on them that recognize the FcG portion
The igA found in breast milk
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

13. What bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
TGF beta and IL 10
Para aortic
Thrombocytopenia

14. What is the defect in hyper IgM syndrome? What are the lab results?
Wiskott Aldrich syndrome
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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

15. What is the clinical use for azathioprine?
Axillary
Anti TSh receptor
...
CD56

16. IgE has the ___________ in the serum
lowest concentration
Antimicrosomal and antithyroglobulin
Anti glutamate carboxylase and anti insulin
Th2; Th1

17. Type IV hypersensitivity is i...
not Ab mediated
Basophils! THey want IG E class switch!
CRP - C3b - IgM
IL 1 and IL 6

18. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Antihistone
MS
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

19. What are the autoantibodies for sjorgens syndrome?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Anti U1 RNP (ribonucleoprotein)
Anti alpha subunit 3 of collagen on type IV bm
Anti SS- A (anti RO) and Anti SS- B

20. Monomer in circulation - ___ when secreted
dimer
Anti topoisomerase
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
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

21. is IgM an opsonizer?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Negative!
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

22. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Paracortex; viral infection
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

23. What is three common causes of severe combined immunodef? What is the result of all three?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
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

24. What is the clinical use of Muromonab?
The igA found in breast milk
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Immunosuppression after kidney transplantation
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

25. What are the main symptoms of B cell immunodeficiencies?
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
SP infections
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

26. What is digoxin immune Fab used for?
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
Antidote for digoxin intoxication
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
heavy chains

27. In thymic development - What is the positive selection? negative selections?
DM type I and RA
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
When you select for which MHC it will have; take out the lymphs that self react
Recom IL 11; thrombocytopenia

28. where do somatic hypermutation and class switching occur?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
secondary
In the germinal center of secondary follicles (In the paler center)
CD21 on B cells (although there is T cell lymphocytosis in EBV)

29. What is the presentation of Brutons agammaglobulinemia?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Internal iliac
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

30. What does granzyme do? who secretes it?
Its a serine protease that activates apoptosis; NK and CD8
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
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
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

31. What lymph node drains the rectum (above the pectinate line)?
If there is class switching and plasma cell production (that is when memory cells are produced)
Internal iliac
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti alpha subunit 3 of collagen on type IV bm

32. What are the autoantibodies for systemic sclerosis?
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
Alternative splicing of mRNA
Anti topoisomerase
IL 3; supports growth and differentiation of bone marrow stem cells

33. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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 nuclear Antibodies (ANA); Anti dsDNA - anti Smith
A j chain

34. What are some catalase positive organisms?
C5a
Inferior mesenteric
S. aureus - E. Coli - aspergillus
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

35. The Fc region is found on the...
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
dimer
pentamer
carboxy terminal

36. What are the three types of lymphocytes?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
B - T - and NK cells
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

37. How is i Th1 helper cell inhibited?
MHC I; from RER with help of the B2 microglobulin
Cytokine IL 10 secreted by Th2
Carbohydrate
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

38. What happens in a secondary follicle?
IgE
IgM
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

39. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
By transcytosis
Sinusitis - otitis media - pneumonia

40. What are the two signals required for T cells? what happens after?
A - B - C; all the D's
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 :(
Immunoflourescent staining of tissue biopsies
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

41. What are the two signals required for Th1 cells? what happens after then activated?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Carbohydrate
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

42. How does the alternative pathway lead to MAC activation?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
Antimicrosomal and antithyroglobulin
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

43. Which is the main antibody in the delayed or secondary response to an antigen?
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!
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
CRP - C3b - IgM
IgG

44. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Cytokine IL 10 secreted by Th2
SP infections
Antidote for digoxin intoxication

45. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
isotype
Activates Th1 helper cells; Macrophages
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

46. ________ regulate the cell mediated response.
Kill them because they have CD16 on them that recognize the FcG portion
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
Humoral
IgG

47. What are the three types of APCs?
Immunoflourescent staining of tissue biopsies
opsonizes
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Macrophages - Dendritic cells - B cells

48. Which disease is associated with B8?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Graves
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

49. What are the cell surface proteins for Macrophages? which two are for opsonins?
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
Delayed type hypersensitivity
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

50. Which is the most abundant antibody in blood?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
MS
...
IgG