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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. which interleukin receptor is required for NK development? activation?
IL 15; IL 12 - interferon Beta and interferon alpha
Celiac
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
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

2. in which immunodef order do you see a lot of pus? no pus?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Anti topoisomerase
Fab portion
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

3. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Wiskott Aldrich syndrome
Paracortex; viral infection
IgAs in mothers breast milk!
If there is class switching and plasma cell production (that is when memory cells are produced)

4. What is epo used for?
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
Anemias (esp due to renal failure)
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
Popliteal

5. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
opsonizes
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

6. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
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
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
Anti mitochondrial

7. What does IL 5 do?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Paracortex
Immunoflourescent staining of tissue biopsies
Celiac

8. What are the two signals required for B cell class switching? Which is the second signal?
A chemotactic factor for neutrophils
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Bind FcG for antibody dependent cellular cytotoxicity

9. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti alpha subunit 3 of collagen on type IV bm
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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

10. What does IL 10 do? who is secreted by?
Superficial inguinal
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Not thymus - BM

11. What are the autoantibodies for wegeners granulomatosis?
Local infection/inflammation; infection of the ln itself; metastasis
IL 4 - 5 - 10 - 6
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Graves

12. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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
Inferior mesenteric
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

13. Which are the only two antiinflammatory cytokines?
T cell precursor
Viral neutralization of igM and 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
TGF beta and IL 10

14. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Anti smooth muscle

15. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Anemias (esp due to renal failure)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
C5a
Interferon gamma and IL 2

16. What is serum sickness? give an example.
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

17. What are target cells?
No because no peptide fragment!
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)
Cells that stil have weird parts of their membrane that macrophages usually bite off
Anti IF

18. Monomer in circulation - ___ when secreted
SP infections
Cross link
dimer
MHC I; from RER with help of the B2 microglobulin

19. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Graves
Yes

20. Which antibodies can be multimeric?
IgM and IgA
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
mesenchymal
Anti IF

21. 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)
Local infection/inflammation; infection of the ln itself; metastasis
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Anti TSh receptor

22. What is the toxicity of azathioprine?
Severe pyogenic infections early in life
Local infection/inflammation; infection of the ln itself; metastasis
...
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

23. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
secondary
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IgM and IgG
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

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?
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Bind FcG for antibody dependent cellular cytotoxicity

25. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
Humoral
Immunoflourescent staining of tissue biopsies
acute phase reactants

26. What links the adaptive and innate immunity?
Complement activation (active in both)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
IgM and IgA
Histamine; post capillary venules - vasodilation

27. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Cells that stil have weird parts of their membrane that macrophages usually bite off
pathogenesis
Rheumatic arthritis
Graves

28. What lymph node drains the stomach?
All MHC 1/CD8
Celiac
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 :(
Activates Th1 helper cells; Macrophages

29. From where do cytokines come from?
Activate macrophages
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
IgG
Lymphocytes

30. What are the autoantibodies for Mixed connective tissue disease?
IgE
Anti U1 RNP (ribonucleoprotein)
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
opsonizes

31. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion

32. What are the autoantibodies for graves?
Anti TSh receptor
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
IL 3; supports growth and differentiation of bone marrow stem cells
Barrel hoop basement membrane fenestrations

33. What is oprelevkin? and What is it used for?
Anti U1 RNP (ribonucleoprotein)
Recom IL 11; thrombocytopenia
secondary
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

34. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Histamine; post capillary venules - vasodilation
IL 4
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

35. ________ regulate the cell mediated response.
Alternative splicing of mRNA
Humoral
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
TNF alpha and IL1

36. 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
Th cells fail to produce interferon gamma; a lot of IgE
Secretory component
TNF alpha and IL1

37. What is recomb gamma interferon used for?
S. aureus - E. Coli - aspergillus
Chronic granulomatous disease
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Paracortex

38. What are the autoantibodies for Celiac disease?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Anti IF

39. What do mature naive B lymphocytes express?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IL 3; supports growth and differentiation of bone marrow stem cells
Th2; Th1
IgM and IgD

40. give an example of how influenza does a major antigenic shift.
By transcytosis
RNA segment reassortment
opsonizes
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

41. What are the autoantibodies for systemic sclerosis?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Anti topoisomerase
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
heavy chains

42. What is thrombopoietin used for?
Thrombocytopenia
IgG
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

43. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
By transcytosis
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Glycoproteins; HLA

44. Only the _______ contribute to the Fc region
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IgM and IgG
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
heavy chains

45. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
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
cannot cross placenta

46. What is the cause of thymic aplasia? What is its presentation? What are the labs?
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
encapsulated
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Popliteal

47. which antibodies can bind complement?
lowest concentration
Antibody mediated cytotoxicity; either complement dependent or complement independent
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgM and IgG

48. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Interferon gamma and IL 2
opsonizes
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
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

49. In general What are T cells good for?
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
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti viral and anti tumor
Stimulate the liver to release acute phase reactants

50. Complements are...
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Hemochromatosis
Paracortex
acute phase reactants