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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 are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
Its a serine protease that activates apoptosis; NK and CD8
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

2. What happens in a deficiency of C3?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
type four
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

3. Which diseases are associated with DR5?
Para aortic
Pernicious Anemia and Hashimotos
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
Anti mitochondrial

4. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
In the germinal center of secondary follicles (In the paler center)
Rheumatic arthritis

5. The alternative pathway is the only constutively...
active complement pathway
A - B - C; all the D's
Activates cytotoxic CD 8 T cells as second signal
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

6. what characterizes an arthus reaction?
Edema and necrosis in that region
S. aureus - E. Coli - aspergillus
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
IgM and IgA

7. What is an example of a parasite showing antigenic variation?
Anti SS- A (anti RO) and Anti SS- B
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
The patient could become cyanotic in the OR!

8. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
TNF alpha and IL1
mesenchymal
Cross link

9. What is the marginal zone of the spleen? what happens there?
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
IgM
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
Secretory component

10. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Barrel hoop basement membrane fenestrations
opsonizes
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

11. What is colostrum?
The igA found in breast milk
T cell activation; no with CD 4 or CD 8
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

12. What are the autoantibodies for other vasculitides?
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

13. What are some catalase positive organisms?
Antimicrosomal and antithyroglobulin
IL 4
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
S. aureus - E. Coli - aspergillus

14. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
Anti Jo -1
T cell activation; no with CD 4 or CD 8
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

15. What do mature naive B lymphocytes express?
IgM and IgD
Internal iliac
All MHC 1/CD8
Anti smooth muscle

16. How is the thymus organized? what happens in each section?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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

17. What is the main function of IL 12? other than macrophages who else can release IL 12?
Complement activation (active in both)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

18. Type Iv hypersensitivity is...
delayed!
Para aortic
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)

19. 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?
Anti topoisomerase
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
delayed!
mesenchymal

20. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
type four
IgM and IgA

21. Which diseases are associated with DR4?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
DM type I and RA
IgE
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

22. What are target cells?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IL 3; supports growth and differentiation of bone marrow stem cells
Cells that stil have weird parts of their membrane that macrophages usually bite off
IgE

23. What are the autoantibodies for goodpastures syndrome?
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
Anti alpha subunit 3 of collagen on type IV bm
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 :(
Interferon gamma and IL 2

24. What is three common causes of severe combined immunodef? What is the result of all three?
Sinusitis - otitis media - pneumonia
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Viral neutralization of igM and IgG!

25. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Cross link
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
secondary
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

26. Monomer in circulation - ___ when secreted
dimer
Type IV
Anti Jo -1
neutrophilia!

27. Describe complement dependent Type II hypersensitivity. Give an example.
Remove encapsulated bacateria
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
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
Histamine; post capillary venules - vasodilation

28. What does granulysin do?
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 :(
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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

29. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
dimer
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
neutrophilia!
Liver! (they are proteins circulating in the blood)

30. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Celiac
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
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
opsonizes

31. What are the two signals required for B cell class switching? Which is the second signal?
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
MS - hay fever - SLE - goodpastures
CD21 on B cells (although there is T cell lymphocytosis in EBV)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

32. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

33. which B and T cell disorder presents with specifically low IgM?
IgA
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Viral neutralization of igM and IgG!
Wiskott Aldrich syndrome

34. which antibodies prevent antigens from binding mucosal surfaces?
Inferior mesenteric
IgM
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

35. what prevents NK cells from killing normal cells if their default is to kill?
Local infection/inflammation; infection of the ln itself; metastasis
Secretory component
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
MHC class molecules bind to KIRS or CD94 to prevent killing

36. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
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
Receiving preformed Antibodies
...
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

37. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

38. What is the general structure of an Ab?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
False! B cell class switching requires a second signal
2 heavy chains and two light chains
IL 3; supports growth and differentiation of bone marrow stem cells

39. What is recomb alpha interferon used for?
IgAs in mothers breast milk!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
CD21 on B cells (although there is T cell lymphocytosis in EBV)

40. What does granzyme do? who secretes it?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Its a serine protease that activates apoptosis; NK and CD8
S. aureus - E. Coli - aspergillus

41. The two heavy chains of an antibody contribute to the...
Immunoflourescent staining of tissue biopsies
Hereditary angioedema; PNH
RNA segment reassortment
Fab portion

42. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Anti topoisomerase
Macrophages - Dendritic cells - B cells
IL 5
Cross link

43. Which disease is associated with HLA A3?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Complement activation (active in both)
Anti viral and anti tumor
Hemochromatosis

44. What are the autoantibodies for drug induced lupus?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Increases expression of MHC I and MHC II and also activates NK cells
acute phase reactants
Antihistone

45. The Fc region is found on the...
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
carboxy terminal
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 4 - 5 - 10 - 6

46. What happens in a secondary follicle?
MHC I; from RER with help of the B2 microglobulin
If there is class switching and plasma cell production (that is when memory cells are produced)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti Ach receptor

47. What are the main symptoms of T cell immunodeficiencies?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
mesenchymal
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

48. How is the antigen loaded onto a MHC II?
SP infections
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
Negative!
delayed!

49. The secondary follicles have __________; primary follicles are dense
pale central germinal centers
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
Delayed type hypersensitivity

50. what happens in a deficiency of C1 esterase inhibitor? DAF?
mesenchymal
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Hereditary angioedema; PNH
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