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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?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Immunosuppression after kidney transplantation
Negative!
A j chain

2. which cytokine inhibits TH2 cells? secreted by who?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IgG
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
Interferon gamma; Th1

3. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Rheumatic arthritis
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

4. What links the adaptive and innate immunity?
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
Popliteal
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Complement activation (active in both)

5. What lymph node drains the thigh?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Superficial inguinal
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
neutrophilia!

6. Which antibody mediates immunity to worms? how?
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Negative nitroblue tetrazolium reduction test
IgE; by activating eosinophils

7. What is the mechanism for sirolimus? what else it known as?
Anti glutamate carboxylase and anti insulin
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
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

8. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
Inferior mesenteric
encapsulated
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

9. In thymic development - What is the positive selection? negative selections?
The patient could become cyanotic in the OR!
When you select for which MHC it will have; take out the lymphs that self react
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
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

10. 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
Interferon gamma; Th1
...
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

11. What bugs can actually infect the lymph node itself?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Yes
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

12. Give three examples of bacteria that use antigenic variation and how.
IgA
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
MS - hay fever - SLE - goodpastures

13. What are the autoantibodies for wegeners granulomatosis?
Negative!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Edema and necrosis in that region
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

14. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
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
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
Hemochromatosis

15. What are the PALS?
Superficial inguinal
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

16. What lymph node drains the breast?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
NK cells
Anti glutamate carboxylase and anti insulin
Axillary

17. What are the main cell surface proteins on B cells?
Anti TSh receptor
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

18. Which diseases are associated with DR2?
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
MS - hay fever - SLE - goodpastures
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

19. What type of side chains are found on Fc region of an antibody?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
pentamer
Carbohydrate
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

20. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Acts as second signal on B cells to induce class switching to IgE and IgG
Negative selection

21. Which disease is associated with DR3?
DM type I
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

22. which interleukin receptor is required for NK development? activation?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Anti mitochondrial
IL 15; IL 12 - interferon Beta and interferon alpha
TLR ad nuclear receptors

23. What are the two signals to kill for NK cells?
Carbohydrate
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Cyclosporine - OKT3
IL 15; IL 12 - interferon Beta and interferon alpha

24. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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
Activates Th1 helper cells; Macrophages

25. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
DM type I
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

26. which of the hypersensitivity reactions is not Ab mediated?
Inferior mesenteric
TNF alpha and IL1
Immunoflourescent staining of tissue biopsies
Type IV

27. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
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
Interferon gamma; Th1
CRP - C3b - IgM
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

28. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
TGF beta and IL 10
TLR ad nuclear receptors
dimer
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

29. Which helper T cells' development is induced by IL 4? IL 12?
Local infection/inflammation; infection of the ln itself; metastasis
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Th2; Th1

30. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activate macrophages
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Recom IL 11; thrombocytopenia

31. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
Anti mitochondrial
CD21 on B cells (although there is T cell lymphocytosis in EBV)

32. IgE has the ___________ in the serum
Chronic granulomatous disease
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
lowest concentration
SP infections

33. What does it mean if there are igM in the serum at birth?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
heavy chains
Liver! (they are proteins circulating in the blood)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

34. What is the main cytokine that activates eosinophils?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IL 5
Anti topoisomerase
Rheumatic arthritis

35. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
No because no peptide fragment!
Active; passive - fast but short half life (3 weeks!)
Antibody mediated cytotoxicity; either complement dependent or complement independent

36. What lymph node drains the upper limb?
IgA
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Axillary
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

37. In general What are T cells good for?
Anti viral and anti tumor
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Increases expression of MHC I and MHC II and also activates NK cells
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

38. What is the presentation of common variable immunodef? and What are the labs?
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
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
not Ab mediated
Steroid responsive nephrotic syndrome

39. What is recomb beta interferon used for?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (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
MS

40. What lymph node drains the anal canal (below the pectinate line)?
TGF beta and IL 10
MHC I - CD16 - CD56
Receiving preformed Antibodies
Superficial inguinal

41. when can graft versus host disease? What is the result?
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
A recomb cytokine of IL 2; RCC and metastatic melanoma
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

42. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
neutrophilia!
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

43. is IgM an opsonizer?
Immunoflourescent staining of tissue biopsies
Negative!
not Ab mediated
Popliteal

44. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
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
Humoral
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
carboxy terminal

45. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
MHC II - B7
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
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

46. What is thrombopoietin used for?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Thrombocytopenia
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
Increases expression of MHC I and MHC II and also activates NK cells

47. From where do cytokines come from?
Lymphocytes
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Anti mitochondrial

48. other than C3a - what other complement acts as an anaphyloxin?
Anemias (esp due to renal failure)
C5a
Anti topoisomerase
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

49. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
2 heavy chains and two light chains
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
Antidote for digoxin intoxication

50. What is recomb alpha interferon used for?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
IgE
TLR ad nuclear receptors