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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. The secondary follicles have __________; primary follicles are dense
Histamine; post capillary venules - vasodilation
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
TGF beta and IL 10
pale central germinal centers

2. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
A recomb cytokine of IL 2; RCC and metastatic melanoma
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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!

3. What is the presentation of Brutons agammaglobulinemia?
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
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

4. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
When you select for which MHC it will have; take out the lymphs that self react
type four

5. What kinds of receptors activate innate immunity?
T cell activation; no with CD 4 or CD 8
MHC II - B7
delayed!
TLR ad nuclear receptors

6. What is the main cytokine that activates eosinophils?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IL 5
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

7. Which diseases are associated with DR4?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Steroid responsive nephrotic syndrome
DM type I and RA

8. Which disease is associated with HLA A3?
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Hemochromatosis
Viral neutralization of igM and IgG!

9. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Steroid responsive nephrotic syndrome
IgA
secondary
Cross link

10. Monomer in circulation - ___ when secreted
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
dimer
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

11. What lymph node drains the breast?
Axillary
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Cytokine IL 10 secreted by Th2

12. What lymph node drains the sigmoid colon?
Inferior mesenteric
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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!
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti

13. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
...
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

14. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Hereditary angioedema; PNH
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Anti Jo -1

15. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
TNF alpha and IL1
IgM and IgG
Bind FcG for antibody dependent cellular cytotoxicity

16. What are howell jolly bodies?
Axillary
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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

17. other than eat and bite RBCs what else do Macrophages of spleen do>
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)
pathogenesis
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Remove encapsulated bacateria

18. 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
Influenza; antigenic shift; antigenic drift
Superficial inguinal
If there is class switching and plasma cell production (that is when memory cells are produced)

19. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

20. describe the classic complement pathway.
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

21. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Fab portion
Celiac
Anti viral and anti tumor

22. What is Aldesleukin? What is it used for
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
T cell activation; no with CD 4 or CD 8
DM type I
A recomb cytokine of IL 2; RCC and metastatic melanoma

23. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
TGF beta and IL 10
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Anti TSh receptor

24. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
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
IgA
Kill them because they have CD16 on them that recognize the FcG portion
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

25. What type of fenestrations are found in the red pulp of the spleen?
Barrel hoop basement membrane fenestrations
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
Axillary
Activate macrophages

26. For which toxins are preformed antibodies (passive) given?
Tetanus - Botulinum - HBV - Rabies
Anti Ach receptor
Remove encapsulated bacateria
Cells that stil have weird parts of their membrane that macrophages usually bite off

27. What is the autoantibody for SLE that is nonspecific? Specific?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
heavy chains
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

28. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
pale central germinal centers
lowest concentration
IgA

29. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
MS
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
By transcytosis

30. What are the autoantibodies for graves?
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 TSh receptor
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
All MHC 1/CD8

31. To what disease do the autoantibodies to IgG (rheumatoid factor)?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Rheumatic arthritis
Celiac
Anti viral and anti tumor

32. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
Antibody mediated cytotoxicity; either complement dependent or complement independent
Secretory component
Liver! (they are proteins circulating in the blood)

33. other than C3a - what other complement acts as an anaphyloxin?
No because no peptide fragment!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
C5a
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

34. Which MHC presents intracellular peptides? how so?
A - B - C; all the D's
Negative selection
MHC I; from RER with help of the B2 microglobulin
acute phase reactants

35. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
MS
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Edema and necrosis in that region

36. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
T
Anti topoisomerase

37. What is the pathogenesis of a candida skin test?
DM type I
Delayed type hypersensitivity
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
acute phase reactants

38. What is recomb alpha interferon used for?
The patient could become cyanotic in the OR!
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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

39. What are the PALS?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IgG

40. What is oprelevkin? and What is it used for?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Recom IL 11; thrombocytopenia
Cyclosporine - OKT3
Interferon gamma and IL 2

41. The alternative pathway is the only constutively...
active complement pathway
mesenchymal
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
isotype

42. What is the toxicity of muromonab?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Its a serine protease that activates apoptosis; NK and CD8
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

43. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
dimer
Histamine; post capillary venules - vasodilation
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

44. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
DM type I
All MHC 1/CD8

45. What are the autoantibodies for polymyositis and dermatomyositis?
lowest concentration
SP infections
Paracortex; viral infection
Anti Jo -1

46. where are complements produced?
Liver! (they are proteins circulating in the blood)
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
IgE

47. which antibodies prevent antigens from binding mucosal surfaces?
Th cells fail to produce interferon gamma; a lot of IgE
type four
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
IgA

48. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
not Ab mediated

49. What is the pathology seen in chronic transplant rejection?
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
Anti glutamate carboxylase and anti insulin
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
The patient could become cyanotic in the OR!

50. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
The patient could become cyanotic in the OR!
Macrophages - Dendritic cells - B cells