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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 is the clinical use of Muromonab?
B - T - and NK cells
By transcytosis
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
Immunosuppression after kidney transplantation

2. What are the autoantibodies for Celiac disease?
Anti IF
IL 4
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
mesenchymal

3. What lymph node drains the breast?
Axillary
A recomb cytokine of IL 2; RCC and metastatic melanoma
Fc
Increases expression of MHC I and MHC II and also activates NK cells

4. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
IL 5
Cytokine IL 10 secreted by Th2
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
pathogenesis

5. What lymph node drains the upper limb?
IL 4
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
Axillary
Kill them because they have CD16 on them that recognize the FcG portion

6. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
...
lowest concentration
TLR ad nuclear receptors
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

7. What are the cell surface proteins on NK cells?
except hyperacute
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
MHC I - CD16 - CD56

8. is IgM an opsonizer?
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
Paracortex; viral infection
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Negative!

9. Describe the capsular structure of a lymph node; What are the functions of the LN?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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 U1 RNP (ribonucleoprotein)

10. How do you test for chronic granulomatous disease?
Basophils! THey want IG E class switch!
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
C5a
Negative nitroblue tetrazolium reduction test

11. What is the pathology in hyperacute transplant rejection?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IgA
SP infections
Humoral

12. Describe complement dependent Type II hypersensitivity. Give an example.
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
Remove encapsulated bacateria
Cytokine IL 10 secreted by Th2
Popliteal

13. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Anti Ach receptor
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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

14. which type of immunity is slow but long lasting? as opposed to...
In the germinal center of secondary follicles (In the paler center)
Graves
Active; passive - fast but short half life (3 weeks!)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

15. can igG cross the placenta?
Hereditary angioedema; PNH
Interferon gamma and IL 2
Yes
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

16. Which are the only two antiinflammatory cytokines?
Daclizumab; prevent ACUTE rejection of renal transplant
By transcytosis
A j chain
TGF beta and IL 10

17. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
MS
Activate macrophages
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

18. What are some catalase positive organisms?
cannot cross placenta
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Paracortex; viral infection
S. aureus - E. Coli - aspergillus

19. What are the three types of lymphocytes?
B - T - and NK cells
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

20. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
IL 5
Superficial inguinal
False! B cell class switching requires a second signal

21. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
IgG
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

22. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
DM type I and RA
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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

23. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Its a serine protease that activates apoptosis; NK and CD8
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Axillary

24. where do somatic hypermutation and class switching occur?
Anti topoisomerase
In the germinal center of secondary follicles (In the paler center)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Its main effect is a defect in Ab opsonization for killing

25. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Humoral
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

26. What is passive immunity?
Receiving preformed Antibodies
Anti viral and anti tumor
IgE
Increases expression of MHC I and MHC II and also activates NK cells

27. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Yes
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Glycoproteins; HLA

28. Which antibody mediates immunity to worms? how?
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
The igA found in breast milk
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
IgE; by activating eosinophils

29. 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?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
MS - hay fever - SLE - goodpastures

30. What is the common variable immunodeficiency ? How is it different from Brutons?
CRP - C3b - IgM
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Edema and necrosis in that region

31. which cytokine inhibits TH2 cells? secreted by who?
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
Activates cytotoxic CD 8 T cells as second signal
Interferon gamma; Th1
Increases expression of MHC I and MHC II and also activates NK cells

32. What does interferon gamma do? What two type of cells does it attack mostly?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
neutrophilia!
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

33. What is the pathogenesis of HyperIgE syndrome? What are the labs?
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
Th cells fail to produce interferon gamma; a lot of IgE
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
C5a

34. What lymph node drains the lateral side of the dorsum of the foot?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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
Popliteal

35. Which disease is associated withB B27?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Superficial inguinal
A recomb cytokine of IL 2; RCC and metastatic melanoma
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

36. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
IL 4 - 5 - 10 - 6
pale central germinal centers

37. So antibodies are the effectors for the humoral response. List some of their functions.
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Paracortex; viral infection
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

38. The idiotype; the Fc portion determines the...
isotype
Anti topoisomerase
Glycoproteins; HLA
MHC II - B7

39. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Th2; Th1
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Carbohydrate

40. Which is the main antibody that provides passive immunity to infants?
Remove encapsulated bacateria
Tetanus - Botulinum - HBV - Rabies
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgG

41. What is hereditary angioedema? What are the C3 levels?
Kill them because they have CD16 on them that recognize the FcG portion
Paracortex
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
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

42. What is immune complex disease? give an example.
MS - hay fever - SLE - goodpastures
Receiving preformed Antibodies
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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

43. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
acute phase reactants

44. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
MHC class molecules bind to KIRS or CD94 to prevent killing
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

45. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Negative!
Anti Ach receptor
Antibody mediated cytotoxicity; either complement dependent or complement independent

46. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
False! B cell class switching requires a second signal
Kill them because they have CD16 on them that recognize the FcG portion
Activates Th1 helper cells; Macrophages

47. What does IgA pick up from epithelial cells before being secreted?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Secretory component
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

48. What is the presentation of Brutons agammaglobulinemia?
Anti Jo -1
IgA
C5a
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

49. 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
Activates Th1 helper cells; Macrophages
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 U1 RNP (ribonucleoprotein)

50. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Alternative splicing of mRNA
IgM and IgA
Not thymus - BM