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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 is recomb alpha interferon used for?
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
Paracortex; viral infection
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

2. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Histamine; post capillary venules - vasodilation
T
Anti Jo -1

3. What portion of the lymph node is not well developed in DiGeorge Syndrome?
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
Carbohydrate
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Paracortex

4. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
IgM
Yes
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

5. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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!
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
T cell dysfunction

6. What is the main function of TNF alpha? How does it do this?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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
2 heavy chains and two light chains

7. What are the autoantibodies for systemic sclerosis?
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
Anti topoisomerase
SP infections
By transcytosis

8. ________ regulate the cell mediated response.
Humoral
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
CD56
IL 15; IL 12 - interferon Beta and interferon alpha

9. What lymph node drains the stomach?
Anti alpha subunit 3 of collagen on type IV bm
...
Celiac
Barrel hoop basement membrane fenestrations

10. Name 5 ways Antibody diversity is generated?
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
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
Daclizumab; prevent ACUTE rejection of renal transplant
Glycoproteins; HLA

11. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
MS - hay fever - SLE - goodpastures
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
lowest concentration

12. which antibody activate mast cells - basophils - and eosinophils?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
MS - hay fever - SLE - goodpastures
IgE

13. Monomer in circulation - ___ when secreted
Sinusitis - otitis media - pneumonia
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
dimer

14. What are some sinopulmonary infections?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Sinusitis - otitis media - pneumonia
Anti glutamate carboxylase and anti insulin
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

15. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
MHC II - B7
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IgG

16. which of the transplant rejections is antibody mediated? why does it occur?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
isotype
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti topoisomerase

17. What does IL 4 do?
Steroid responsive nephrotic syndrome
Anti SS- A (anti RO) and Anti SS- B
Acts as second signal on B cells to induce class switching to IgE and IgG
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

18. What is the most common selective Ig deficiency? What is the presentation?
TLR ad nuclear receptors
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
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Remove encapsulated bacateria

19. Which is the main antibody that provides passive immunity to infants?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti U1 RNP (ribonucleoprotein)
IgG
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

20. What is filgrastim and sargramostim? and What is it used for?
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 :(
Paracortex; viral infection
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IgM and IgG

21. What are the autoantibodies for sjorgens syndrome?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Activates cytotoxic CD 8 T cells as second signal
Anti SS- A (anti RO) and Anti SS- B
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

22. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Interferon gamma; Th1
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

23. What is the toxicity of azathioprine?
...
DM type I and RA
Macrophages - Dendritic cells - B cells
pale central germinal centers

24. 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?
Immunosuppression after kidney transplantation
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Wiskott Aldrich syndrome

25. What is chronic mucocutaneous candidiasis d/t?
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
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
Active; passive - fast but short half life (3 weeks!)
T cell dysfunction

26. What is the main cytokine released by T cells? What does it do
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IL 3; supports growth and differentiation of bone marrow stem cells
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
acute phase reactants

27. Which diseases are associated with DR2?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
MS - hay fever - SLE - goodpastures
Negative selection
except hyperacute

28. What are the autoantibodies for goodpastures syndrome?
opsonizes
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anti alpha subunit 3 of collagen on type IV bm

29. What are the major functions of Antibodies?
Acts as second signal on B cells to induce class switching to IgE and IgG
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
A chemotactic factor for neutrophils

30. other than C3a - what other complement acts as an anaphyloxin?
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
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 :(
C5a
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

31. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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

32. what mediates the type II hypersensitivity? What are the two different methods?
neutrophilia!
Antibody mediated cytotoxicity; either complement dependent or complement independent
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

33. What are the autoantibodies for type I diabetes mellitus?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Bind FcG for antibody dependent cellular cytotoxicity
Anti glutamate carboxylase and anti insulin

34. Which helper T cells' development is induced by IL 4? IL 12?
Th2; Th1
Anti Jo -1
pentamer
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

35. What is the clinical use for azathioprine?
Macrophages - Dendritic cells - B cells
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
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
...

36. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Superior mesenteric
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
False! B cell class switching requires a second signal
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

37. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Anti IF
Edema and necrosis in that region
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

38. where are complements produced?
Liver! (they are proteins circulating in the blood)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
Fc

39. What is serum sickness? give an example.
Remove encapsulated bacateria
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
Viral neutralization of igM and IgG!

40. Which type of selection of thymic development provides central tolerance?
Negative selection
Fab portion
False! B cell class switching requires a second signal
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

41. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Activates cytotoxic CD 8 T cells as second signal

42. What is the general structure of an Ab?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
mesenchymal
In the germinal center of secondary follicles (In the paler center)
2 heavy chains and two light chains

43. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

44. What is the receptor for EBV? On what cells is that located?
Superficial inguinal
MS
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)

45. What is the pathogenesis of a hypersensitivity reaction?
A - B - C; all the D's
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
IgG
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

46. What does IgA pick up from epithelial cells before being secreted?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
IL 4
Secretory component

47. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
...
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

48. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Cyclosporine - OKT3
Th2; Th1

49. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
Active; passive - fast but short half life (3 weeks!)
isotype
Negative selection

50. What are the autoantibodies for other vasculitides?
MS
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
CD56