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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. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
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
except hyperacute
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Anti SS- A (anti RO) and Anti SS- B

2. What do mature naive B lymphocytes express?
Negative selection
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IgM and IgD
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

3. which antibody activate mast cells - basophils - and eosinophils?
IgE
IgG
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
A chemotactic factor for neutrophils

4. what will NK cells do to cells covered in IgG Ab? why?
Kill them because they have CD16 on them that recognize the FcG portion
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Active; passive - fast but short half life (3 weeks!)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

5. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Receiving preformed Antibodies
MHC II - B7
A j chain

6. 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).
2 heavy chains and two light chains
IgE
Daclizumab; prevent ACUTE rejection of renal transplant
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!

7. What does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IgG
IgE
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

8. The lymphocytes are ________ origin
IgG
Fc
Anti glutamate carboxylase and anti insulin
mesenchymal

9. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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 chemotactic factor for neutrophils

10. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
pathogenesis
Superficial inguinal
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

11. What is the pathogenesis of a candida skin test?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Delayed type hypersensitivity
Negative selection

12. To what portion of the Antibody do the complements bind?
IgM and IgD
Interferon gamma; Th1
Fc
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

13. Name two endogenous pyrogens
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IL 1 and IL 6
Tetanus - Botulinum - HBV - Rabies
Liver! (they are proteins circulating in the blood)

14. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
IgAs in mothers breast milk!
SP infections
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h

15. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
False! B cell class switching requires a second signal
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
Anti topoisomerase
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

16. describe the pathogenesis of delayed type IV hypersensitivity
Bind FcG for antibody dependent cellular cytotoxicity
Kill them because they have CD16 on them that recognize the FcG portion
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
type four

17. where are complements produced?
Anti Jo -1
IgE
Anti viral and anti tumor
Liver! (they are proteins circulating in the blood)

18. In thymic development - What is the positive selection? negative selections?
A chemotactic factor for neutrophils
When you select for which MHC it will have; take out the lymphs that self react
IgE
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

19. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Graves
DM type I and RA
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

20. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
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
T cell precursor
Daclizumab; prevent ACUTE rejection of renal transplant
IgM and IgG

21. What cytokines are released by Th1 cells?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Macrophages - Dendritic cells - B cells
Interferon gamma and IL 2

22. other than C3a - what other complement acts as an anaphyloxin?
C5a
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
...
2 heavy chains and two light chains

23. What are the T cell functions?
Histamine; post capillary venules - vasodilation
Th cells fail to produce interferon gamma; a lot of IgE
Superior mesenteric
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

24. What do multimeric antibodies require for assembly?
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
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
2 heavy chains and two light chains
A j chain

25. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
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
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
Antibody mediated cytotoxicity; either complement dependent or complement independent

26. where do somatic hypermutation and class switching occur?
pathogenesis
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
In the germinal center of secondary follicles (In the paler center)

27. which antibody is involved in the primary response or immediate response to an antigen?
dimer
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
IgM
NK cells

28. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
heavy chains
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
neutrophilia!

29. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Not thymus - BM
Paracortex; viral infection
Chronic granulomatous disease
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

30. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
Anti topoisomerase
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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

31. A lymph node is a ________ lymphoid organ.
secondary
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
Celiac
IL 3; supports growth and differentiation of bone marrow stem cells

32. Type IV hypersensitivity is i...
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
not Ab mediated
Kill them because they have CD16 on them that recognize the FcG portion
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

33. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti alpha subunit 3 of collagen on type IV bm
not Ab mediated

34. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
Anti Jo -1
IgM and IgA
Influenza; antigenic shift; antigenic drift

35. How fast does it occur?
IgE
IL 1 and IL 6
The patient could become cyanotic in the OR!
Activates Th1 helper cells; Macrophages

36. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
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
Activates Th1 helper cells; Macrophages
IL 5

37. 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?
delayed!
pale central germinal centers
T cell dysfunction
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

38. Which type of selection of thymic development provides central tolerance?
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
Superior mesenteric
Negative selection
Recom IL 11; thrombocytopenia

39. The secondary follicles have __________; primary follicles are dense
A j chain
pale central germinal centers
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Influenza; antigenic shift; antigenic drift

40. What are the autoantibodies for sjorgens syndrome?
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
Popliteal
Inferior mesenteric
Anti SS- A (anti RO) and Anti SS- B

41. What lymph node drains the duodenum - jejunum?
Superior mesenteric
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

42. What is the general structure of an Ab?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
The patient could become cyanotic in the OR!
2 heavy chains and two light chains

43. What kinds of receptors activate innate immunity?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
TLR ad nuclear receptors
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

44. The idiotype; the Fc portion determines the...
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
isotype

45. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

46. How do you test for type III hypersensitivity?
Acts as second signal on B cells to induce class switching to IgE and IgG
Immunoflourescent staining of tissue biopsies
Chronic granulomatous disease
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

47. What lymph node drains the stomach?
Celiac
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Th cells fail to produce interferon gamma; a lot of IgE
IgG

48. What are the autoantibodies for Mixed connective tissue disease?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti U1 RNP (ribonucleoprotein)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

49. What are the autoantibodies for wegeners granulomatosis?
DM type I and RA
...
acute phase reactants
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

50. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Local infection/inflammation; infection of the ln itself; metastasis
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MS - hay fever - SLE - goodpastures
except hyperacute