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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. what will NK cells do to cells covered in IgG Ab? why?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T 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
Type IV
Kill them because they have CD16 on them that recognize the FcG portion

2. What are the autoantibodies for sjorgens syndrome?
Anti SS- A (anti RO) and Anti SS- B
Stimulate the liver to release acute phase reactants
IgA
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

3. What is the presentation of hyperIgM syndrome?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Carbohydrate
Severe pyogenic infections early in life
Cells that stil have weird parts of their membrane that macrophages usually bite off

4. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
TGF beta and IL 10
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IgM

5. What are the autoantibodies for type I diabetes mellitus?
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
Anti glutamate carboxylase and anti insulin
Edema and necrosis in that region
Antimicrosomal and antithyroglobulin

6. What does granzyme do? who secretes it?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Its a serine protease that activates apoptosis; NK and CD8
type four
Influenza; antigenic shift; antigenic drift

7. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Antihistone
Paracortex

8. What are the autoantibodies for other vasculitides?
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
DM type I

9. What can cause a lymph node enlargement?
Activates cytotoxic CD 8 T cells as second signal
Local infection/inflammation; infection of the ln itself; metastasis
Type IV
Basophils! THey want IG E class switch!

10. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
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
pale central germinal centers
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Cytokine IL 10 secreted by Th2

11. The alternative pathway is the only constutively...
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Bind FcG for antibody dependent cellular cytotoxicity
active complement pathway

12. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

13. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Cross link
Local infection/inflammation; infection of the ln itself; metastasis
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

14. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
MHC I - CD16 - CD56
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

15. The two heavy chains of an antibody contribute to the...
Basophils! THey want IG E class switch!
Fab portion
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

16. What is the pathogenesis of a hypersensitivity reaction?
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
Wiskott Aldrich syndrome
IgG
IL 1 and IL 6

17. What is the toxicity of azathioprine?
Chronic granulomatous disease
delayed!
...
Superficial inguinal

18. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
T
delayed!
Alternative splicing of mRNA

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?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Cyclosporine - OKT3
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

20. What is the defect in hyper IgM syndrome? What are the lab results?
Anti viral and anti tumor
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Para aortic

21. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
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
Yes
except hyperacute
DM type I and RA

22. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Glycoproteins; HLA
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

23. 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?
Severe pyogenic infections early in life
When you select for which MHC it will have; take out the lymphs that self react
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
Tetanus - Botulinum - HBV - Rabies

24. can igG cross the placenta?
Yes
Liver! (they are proteins circulating in the blood)
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 :(
TLR ad nuclear receptors

25. How is the thymus organized? what happens in each section?
MS - hay fever - SLE - goodpastures
Anti Ach receptor
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
MHC I - CD16 - CD56

26. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Viral neutralization of igM and IgG!
Glycoproteins; HLA
Receiving preformed Antibodies

27. The secondary follicles have __________; primary follicles are dense
Steroid responsive nephrotic syndrome
pale central germinal centers
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Anti IF

28. What are the cell surface proteins for Macrophages? which two are for opsonins?
Celiac
Humoral
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

29. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
lowest concentration
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
DM type I and RA
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

30. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Cytokine IL 10 secreted by Th2
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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 :(

31. What lymph node drains the testes?
Para aortic
Complement activation (active in both)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

32. To what disease do the autoantibodies to IgG (rheumatoid factor)?
pathogenesis
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Rheumatic arthritis
IL 1 and IL 6

33. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
Antidesmoglein

34. What lymph node drains the sigmoid colon?
Inferior mesenteric
Thrombocytopenia
Interferon gamma; Th1
Receiving preformed Antibodies

35. Describe the capsular structure of a lymph node; What are the functions of the LN?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
A - B - C; all the D's
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

36. is IgM an opsonizer?
DM type I and RA
Negative!
...
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

37. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
Superior mesenteric
active complement pathway
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

38. What is the clinical use of Muromonab?
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
Its main effect is a defect in Ab opsonization for killing
Immunosuppression after kidney transplantation
Edema and necrosis in that region

39. What are the labs in brutons agammaglobulinemia?
When you select for which MHC it will have; take out the lymphs that self react
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti Ach receptor

40. hat is the presentation of Jobs syndrome or Hyper IgE?
Fc
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

41. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Its main effect is a defect in Ab opsonization for killing
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
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

42. What is the clinical use for sirolimus? what should you combine it with?
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

43. What is the most common example of passive immunity?
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
IgAs in mothers breast milk!
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
The igA found in breast milk

44. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
The igA found in breast milk
C5a

45. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
Anti mitochondrial
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

46. How does the alternative pathway lead to MAC activation?
IgG
IL 3; supports growth and differentiation of bone marrow stem cells
Chronic granulomatous 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

47. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
Rheumatic arthritis
Antibody mediated cytotoxicity; either complement dependent or complement independent
Anti SS- A (anti RO) and Anti SS- B

48. What does it mean if there are igM in the serum at birth?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
DM type I and RA

49. What is the toxicity of muromonab?
Axillary
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Severe pyogenic infections early in life
type four

50. What are the two signals to kill for NK cells?
TGF beta and IL 10
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)