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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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1. Only the _______ contribute to the Fc region
Antidote for digoxin intoxication
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
heavy chains
T cell precursor

2. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
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
cannot cross placenta
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

3. What are the major functions of Antibodies?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
CRP - C3b - IgM
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

4. What does IL 4 do?
Not thymus - BM
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Acts as second signal on B cells to induce class switching to IgE and IgG
TLR ad nuclear receptors

5. which type of immunity is slow but long lasting? as opposed to...
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Active; passive - fast but short half life (3 weeks!)
IgM
Its a serine protease that activates apoptosis; NK and CD8

6. The MALT/GALT are not...
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
encapsulated
IgM and IgG
C5a

7. What is a type I hypersensitivity reaction? What is atopic?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
IL 5
Kill them because they have CD16 on them that recognize the FcG portion
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

8. 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?
The igA found in breast milk
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

9. 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
Basophils! THey want IG E class switch!
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

10. From where do cytokines come from?
MS - hay fever - SLE - goodpastures
Lymphocytes
Liver! (they are proteins circulating in the blood)
MS

11. What are the autoantibodies for polymyositis and dermatomyositis?
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
TGF beta and IL 10
neutrophilia!
Anti Jo -1

12. What does IL 5 do?
IgE
TGF beta and IL 10
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
active complement pathway

13. other than mediating shock - what else does TNF alpha do? who releases it mainly?
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)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anemias (esp due to renal failure)
Activates Th1 helper cells; Macrophages

14. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Antimicrosomal and antithyroglobulin
Edema and necrosis in that region
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

15. The secondary follicles have __________; primary follicles are dense
Cyclosporine - OKT3
Superficial inguinal
Immunoflourescent staining of tissue biopsies
pale central germinal centers

16. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
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
Glycoproteins; HLA
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

17. How do you test for chronic granulomatous disease?
Anti U1 RNP (ribonucleoprotein)
Negative nitroblue tetrazolium reduction test
2 heavy chains and two light chains
Hereditary angioedema; PNH

18. What lymph node drains the testes?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Para aortic

19. How is the thymus organized? what happens in each section?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
Popliteal
Steroid responsive nephrotic syndrome

20. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Interferon gamma; Th1
Cyclosporine - OKT3
Local infection/inflammation; infection of the ln itself; metastasis

21. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
NK cells
Acts as second signal on B cells to induce class switching to IgE and IgG
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

22. What is oprelevkin? and What is it used for?
Superior mesenteric
secondary
Recom IL 11; thrombocytopenia
Complement activation (active in both)

23. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Activate macrophages
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
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

24. Name the three opsonins
CRP - C3b - IgM
IL 15; IL 12 - interferon Beta and interferon alpha
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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

25. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
Hemochromatosis
Histamine; post capillary venules - vasodilation
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

26. which antibodies can bind complement?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgM and IgG

27. What are the cell surface proteins on NK cells?
pale central germinal centers
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MHC I - CD16 - CD56
Anti IF

28. What are the mediators that mast cells release?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Sinusitis - otitis media - pneumonia
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
MHC II - B7

29. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
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
Tetanus - Botulinum - HBV - Rabies
Fab portion

30. what prevents NK cells from killing normal cells if their default is to kill?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
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!
MHC class molecules bind to KIRS or CD94 to prevent killing

31. what will NK cells do to cells covered in IgG Ab? why?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IL 4
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Kill them because they have CD16 on them that recognize the FcG portion

32. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Cross link
Anti viral and anti tumor
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

33. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Para aortic
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!

34. What are the autoantibodies for graves?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Th2; Th1
Anti TSh receptor

35. 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)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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

36. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
2 heavy chains and two light chains
T
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Delayed type hypersensitivity

37. What is the main function of IL 8?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Th cells fail to produce interferon gamma; a lot of IgE
A chemotactic factor for neutrophils
IgG

38. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
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)
Daclizumab; prevent ACUTE rejection of renal transplant
delayed!

39. What lymph node drains the breast?
Axillary
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)
Severe pyogenic infections early in life
Fab portion

40. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Its main effect is a defect in Ab opsonization for killing
MHC II - B7
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

41. What kinds of receptors activate innate immunity?
Rheumatic arthritis
TLR ad nuclear receptors
delayed!
IL 5

42. can igG cross the placenta?
Yes
Axillary
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Chronic granulomatous disease

43. What is the main cytokine that activates eosinophils?
...
IL 5
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

44. What are superantigens? give two examples.
Superficial inguinal
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
2 heavy chains and two light chains
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

45. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
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
Alternative splicing of mRNA
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
carboxy terminal

46. What is the clinical use for azathioprine?
Anti Jo -1
...
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

47. What are the autoantibodies for pemphigus bulgaris?
Receiving preformed Antibodies
Activate macrophages
Antidesmoglein
Para aortic

48. What are the labs in brutons agammaglobulinemia?
Anti viral and anti tumor
Cells that stil have weird parts of their membrane that macrophages usually bite off
IL 1 and IL 6
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

49. 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
IL 15; IL 12 - interferon Beta and interferon alpha
except hyperacute

50. What are the autoantibodies for pernicious anemia?
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
Anti SS- A (anti RO) and Anti SS- B
Anti IF
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

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USMLE Step 1 Immunology

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