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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.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.

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. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Wiskott Aldrich syndrome
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Anti IF

2. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
carboxy terminal
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
NK cells
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

3. IgE has the ___________ in the serum
lowest concentration
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
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
IgM

4. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Its a serine protease that activates apoptosis; NK and CD8
IgM
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

5. hat is the presentation of Jobs syndrome or Hyper IgE?
Receiving preformed Antibodies
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
Chronic granulomatous disease

6. What is the presentation of scid? treatment?
dimer
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

7. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

8. The two heavy chains of an antibody contribute to the...
isotype
Fab portion
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 BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

9. What are the main cell surface proteins on B cells?
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
isotype

10. Type Iv hypersensitivity is...
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Cytokine IL 10 secreted by Th2
delayed!
Yes

11. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
active complement pathway
Chronic granulomatous disease
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Previous transfusion; pregnant woman whose fetus had paternal antigens

12. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
MHC class molecules bind to KIRS or CD94 to prevent killing
DM type I and RA
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

13. What is the mechanism for sirolimus? what else it known as?
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
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
MHC II - B7

14. what prevents NK cells from killing normal cells if their default is to kill?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
T cell precursor
Para aortic
MHC class molecules bind to KIRS or CD94 to prevent killing

15. What are the PALS?
Alternative splicing of mRNA
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
A - B - C; all the D's
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

16. What is the main cytokine released by T cells? What does it do
secondary
Paracortex
IL 3; supports growth and differentiation of bone marrow stem cells
Stimulate the liver to release acute phase reactants

17. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
A - B - C; all the D's
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
except hyperacute
IL 1 and IL 6

18. What are target cells?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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

19. How is the antigen loaded onto a MHC II?
Barrel hoop basement membrane fenestrations
IL 4 - 5 - 10 - 6
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
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

20. What is the clinical use of Muromonab?
type four
Basophils! THey want IG E class switch!
Immunosuppression after kidney transplantation
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

21. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
Edema and necrosis in that region
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
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

22. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

23. What are the autoantibodies for drug induced lupus?
heavy chains
Antihistone
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
Kill them because they have CD16 on them that recognize the FcG portion

24. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Active; passive - fast but short half life (3 weeks!)
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

25. what characterizes an arthus reaction?
C5a
encapsulated
MS - hay fever - SLE - goodpastures
Edema and necrosis in that region

26. What is the pathogenesis of HyperIgE syndrome? What are the labs?
Th cells fail to produce interferon gamma; a lot of IgE
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain 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
lowest concentration

27. are Th cells involved in trapping of antigens of endotoxin/LPS?
Superficial inguinal
No because no peptide fragment!
The igA found in breast milk
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

28. What are the autoantibodies for hashimotos?
Kill them because they have CD16 on them that recognize the FcG portion
Antimicrosomal and antithyroglobulin
IL 4
Its main effect is a defect in Ab opsonization for killing

29. What links the adaptive and innate immunity?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MS
Histamine; post capillary venules - vasodilation
Complement activation (active in both)

30. What type of side chains are found on Fc region of an antibody?
Carbohydrate
IgAs in mothers breast milk!
TNF alpha and IL1
encapsulated

31. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Paracortex
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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

32. What is recomb beta interferon used for?
type four
acute phase reactants
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
MS

33. what happens in a deficiency of C1 esterase inhibitor? DAF?
pathogenesis
Hereditary angioedema; PNH
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

34. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
NK cells
Anti smooth muscle
DM type I
TNF alpha and IL1

35. Which antibody mediates immunity to worms? how?
IgE; by activating eosinophils
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
encapsulated
Anti alpha subunit 3 of collagen on type IV bm

36. Give three examples of bacteria that use antigenic variation and how.
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

37. What lymph node drains the thigh?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Superficial inguinal

38. What are some catalase positive organisms?
except hyperacute
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
S. aureus - E. Coli - aspergillus
IL 1 and IL 6

39. when can graft versus host disease? What is the result?
Th cells fail to produce interferon gamma; a lot of IgE
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
RNA segment reassortment

40. other than eat and bite RBCs what else do Macrophages of spleen do>
TGF beta and IL 10
Para aortic
Remove encapsulated bacateria
Activate macrophages

41. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Para aortic
Alternative splicing of mRNA
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
pathogenesis

42. What is immune complex disease? give an example.
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
lowest concentration
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

43. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
IL 1 and IL 6
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
Its main effect is a defect in Ab opsonization for killing

44. What are the main symptoms of B cell immunodeficiencies?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
SP infections
IL 3; supports growth and differentiation of bone marrow stem cells
DM type I

45. Which disease is associated with HLA A3?
Hemochromatosis
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
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
Bind FcG for antibody dependent cellular cytotoxicity

46. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
cannot cross placenta
IgA
Immunosuppression after kidney transplantation

47. other than C3a - what other complement acts as an anaphyloxin?
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!
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
C5a
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

48. What do multimeric antibodies require for assembly?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
A j chain

49. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Humoral
MHC I; from RER with help of the B2 microglobulin
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

50. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Wiskott Aldrich syndrome
Glycoproteins; HLA
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)