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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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Match each statement with the correct term.
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1. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Liver! (they are proteins circulating in the blood)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IL 4 - 5 - 10 - 6

2. Which disease is associated withB B27?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

3. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Cytokine IL 10 secreted by Th2
Rheumatic arthritis
carboxy terminal
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

4. what characterizes an arthus reaction?
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
Inferior mesenteric
Fc
Edema and necrosis in that region

5. How is the antigen loaded onto a MHC II?
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
False! B cell class switching requires a second signal
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

6. Which is the main antibody that provides passive immunity to infants?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IgG
Complement activation (active in both)
except hyperacute

7. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Sinusitis - otitis media - pneumonia
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
All MHC 1/CD8

8. what cell surface proteins are on all APCs?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
MHC II - B7
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Acts as second signal on B cells to induce class switching to IgE and IgG

9. which interleukin receptor is required for NK development? activation?
B - T - and NK cells
IL 15; IL 12 - interferon Beta and interferon alpha
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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

10. The pathogenesis of contact dermatitis is ________ hypersensitivity
Anti TSh receptor
Antihistone
type four
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

11. What are the autoantibodies for type I diabetes mellitus?
DM type I
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anti glutamate carboxylase and anti insulin

12. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
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
Th cells fail to produce interferon gamma; a lot of IgE
CD56
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

13. A lymph node is a ________ lymphoid organ.
secondary
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
IgG
TGF beta and IL 10

14. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

15. What lymph node drains the sigmoid colon?
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
Inferior mesenteric
Th2; Th1
active complement pathway

16. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Activates Th1 helper cells; Macrophages
Activate macrophages
Cross link
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

17. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti glutamate carboxylase and anti insulin
Anti Ach receptor
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

18. Which HLA's are included in MHC I? MHC II?

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19. What is three common causes of severe combined immunodef? What is the result of all three?
RNA segment reassortment
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
pathogenesis

20. Which helper T cells' development is induced by IL 4? IL 12?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Th2; Th1
Not thymus - BM

21. what secretes IL 4?
Basophils! THey want IG E class switch!
Carbohydrate
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
Chronic granulomatous disease

22. describe the classic complement pathway.
type four
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Recom IL 11; thrombocytopenia
Anemias (esp due to renal failure)

23. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
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
Anti topoisomerase
Superficial inguinal

24. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
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
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Negative!

25. what ensure that a memory response is generated?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
If there is class switching and plasma cell production (that is when memory cells are produced)
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

26. What are the two signals required for T cells? what happens after?
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 :(
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
IgG
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

27. Describe the Mannose Lectin pathway
By transcytosis
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
Activates cytotoxic CD 8 T cells as second signal
Type IV

28. What are target cells?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cells that stil have weird parts of their membrane that macrophages usually bite off
MS - hay fever - SLE - goodpastures
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

29. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Steroid responsive nephrotic syndrome
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

30. What are C1 - C2 - C3 - C4 important for?
Immunosuppression after kidney transplantation
isotype
Viral neutralization of igM and IgG!
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

31. What is a type I hypersensitivity reaction? What is atopic?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
T cell dysfunction
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
...

32. Leukocyte adhesion defect presents with...
neutrophilia!
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
Edema and necrosis in that region
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

33. Which antibodies can be multimeric?
Carbohydrate
IgM and IgA
A - B - C; all the D's
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

34. What is the most common selective Ig deficiency? What is the presentation?
Fab portion
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

35. Which diseases are associated with DR4?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Fc
DM type I and RA

36. The alternative pathway is the only constutively...
active complement pathway
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
If there is class switching and plasma cell production (that is when memory cells are produced)
2 heavy chains and two light chains

37. Which disease is associated with HLA A3?
Hemochromatosis
Para aortic
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
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

38. What are MHC's necessary for? By themselves?
DM type I and RA
MHC I; from RER with help of the B2 microglobulin
IL 1 and IL 6
T cell activation; no with CD 4 or CD 8

39. What is Aldesleukin? What is it used for
MHC class molecules bind to KIRS or CD94 to prevent killing
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
A recomb cytokine of IL 2; RCC and metastatic melanoma
2 heavy chains and two light chains

40. What is the most common example of passive immunity?
IgAs in mothers breast milk!
IgM and IgD
IgM and IgA
RNA segment reassortment

41. What is the presentation of hyperIgM syndrome?
Severe pyogenic infections early in life
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Daclizumab; prevent ACUTE rejection of renal transplant
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

42. What are the autoantibodies for primary biliary cirrhosis?
MHC class molecules bind to KIRS or CD94 to prevent killing
CRP - C3b - IgM
IgG
Anti mitochondrial

43. What lymph node drains the duodenum - jejunum?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Superior mesenteric
active complement pathway
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

44. Other than stimulating fever - what else does IL 6 do?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Anti IF
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Stimulate the liver to release acute phase reactants

45. hat is the presentation of Jobs syndrome or Hyper IgE?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

46. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
In the germinal center of secondary follicles (In the paler center)
Influenza; antigenic shift; antigenic drift
IgM and IgG

47. What is the toxicity of muromonab?
T cell dysfunction
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
T cell precursor
Macrophages - Dendritic cells - B cells

48. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Cyclosporine - OKT3
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IgM and IgD

49. 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
Humoral
...
Recom IL 11; thrombocytopenia

50. What does IL 2 do?
Activates cytotoxic CD 8 T cells as second signal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
CD56
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

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USMLE Step 1 Immunology

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