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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 are the two signals required for T cells? what happens after?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

2. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
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
Stimulate the liver to release acute phase reactants

3. What is three common causes of severe combined immunodef? What is the result of all three?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IgAs in mothers breast milk!
A chemotactic factor for neutrophils
TNF alpha and IL1

4. What are the main symptoms of B cell immunodeficiencies?
Stimulate the liver to release acute phase reactants
T cell activation; no with CD 4 or CD 8
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
SP infections

5. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
active complement pathway
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Activates Th1 helper cells; Macrophages

6. What are MHC's necessary for? By themselves?
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
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 activation; no with CD 4 or CD 8
IgG

7. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
Immunoflourescent staining of tissue biopsies
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

8. Describe the complement independent Type II hypersenstivity reaction. Give an example.
A recomb cytokine of IL 2; RCC and metastatic melanoma
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
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

9. What is the main function of TNF alpha? How does it do this?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Yes
Interferon gamma and IL 2

10. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
Celiac
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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

11. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
pathogenesis
TNF alpha and IL1

12. What are the cell surface proteins for Macrophages? which two are for opsonins?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

13. IgM can fix complement but...
encapsulated
cannot cross placenta
Remove encapsulated bacateria
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)

14. describe the classic complement pathway.
Axillary
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anti topoisomerase
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

15. What are the major functions of Antibodies?
Superficial inguinal
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
IgE; by activating eosinophils
carboxy terminal

16. How do you test for chronic granulomatous disease?
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Negative nitroblue tetrazolium reduction test

17. How is sirolimus different from tacrolimus?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Axillary
NK cells

18. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Graves
Cross link
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Interferon gamma; Th1

19. Which diseases are associated with DR2?
MS - hay fever - SLE - goodpastures
T cell dysfunction
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
acute phase reactants

20. can igG cross the placenta?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Yes
Paracortex
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

21. What does IL 2 do?
IL 4 - 5 - 10 - 6
Activates cytotoxic CD 8 T cells as second signal
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

22. What are the cell surface proteins on NK cells?
T cell precursor
...
MHC I - CD16 - CD56
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

23. IgE has the ___________ in the serum
lowest concentration
CD56
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 I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

24. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
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!
A recomb cytokine of IL 2; RCC and metastatic melanoma
Cyclosporine - OKT3
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

25. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
NK cells
IgE
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

26. Which antibody mediates immunity to worms? how?
isotype
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IgE; by activating eosinophils
Immunoflourescent staining of tissue biopsies

27. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
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
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Chronic granulomatous disease

28. Which disease is associated with HLA A3?
secondary
Complement activation (active in both)
Hemochromatosis
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

29. From where do cytokines come from?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
Lymphocytes
Liver! (they are proteins circulating in the blood)

30. Monomer in circulation - ___ when secreted
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
Immunoflourescent staining of tissue biopsies
dimer

31. What are some sinopulmonary infections?
Edema and necrosis in that region
Sinusitis - otitis media - pneumonia
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

32. How does igA cross the epithelium?
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
By transcytosis
Viral neutralization of igM and IgG!
MHC II - B7

33. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is 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
NK cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

34. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
IL 4 - 5 - 10 - 6

35. What is thrombopoietin used for?
IL 1 and IL 6
Thrombocytopenia
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
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

36. What are the autoantibodies for primary biliary cirrhosis?
secondary
Anti mitochondrial
IgAs in mothers breast milk!
A - B - C; all the D's

37. The Fc region is found on the...
Negative nitroblue tetrazolium reduction test
carboxy terminal
pathogenesis
opsonizes

38. What are the labs in brutons agammaglobulinemia?
dimer
CRP - C3b - IgM
secondary
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

39. IgG...
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
opsonizes
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
When you select for which MHC it will have; take out the lymphs that self react

40. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
NK cells
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

41. What are howell jolly bodies?
Axillary
MHC class molecules bind to KIRS or CD94 to prevent killing
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

42. What is hereditary angioedema? What are the C3 levels?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
Paracortex; viral infection
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

43. Which is the most abundant antibody in blood?
IgG
Edema and necrosis in that region
The patient could become cyanotic in the OR!
Superficial inguinal

44. What kinds of receptors activate innate immunity?
RNA segment reassortment
TLR ad nuclear receptors
...
C5a

45. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Axillary
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

46. What does interferon gamma do? What two type of cells does it attack mostly?
IgG
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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!
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

47. other than eat and bite RBCs what else do Macrophages of spleen do>
Thrombocytopenia
Remove encapsulated bacateria
Interferon gamma; Th1
Delayed type hypersensitivity

48. What is the pathology seen in chronic transplant rejection?
Active; passive - fast but short half life (3 weeks!)
Inferior mesenteric
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Internal iliac

49. 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?
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
CD56
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Humoral

50. which B and T cell disorder presents with specifically low IgM?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Axillary
Wiskott Aldrich syndrome
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)