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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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1. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
encapsulated
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
False! B cell class switching requires a second signal
Antihistone

2. What are the major functions of Antibodies?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T 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

3. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

4. What do multimeric antibodies require for assembly?
A j chain
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Steroid responsive nephrotic syndrome
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

5. How does complement link innate and adaptive?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Activate macrophages
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

6. Leukocyte adhesion defect presents with...
The igA found in breast milk
Axillary
neutrophilia!
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

7. What does granzyme do? who secretes it?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Its a serine protease that activates apoptosis; NK and CD8
S. aureus - E. Coli - aspergillus
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

8. What does Interferon alpha and beta do? how?
A j chain
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Complement activation (active in both)

9. what cytokine does basophils secrete?
T cell precursor
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
IL 4
Chronic granulomatous disease

10. IgG...
opsonizes
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
IL 1 and IL 6

11. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
RNA segment reassortment
Antihistone
IL 5

12. Type IV hypersensitivity is i...
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)
not Ab mediated
Severe pyogenic infections early in life
Fab portion

13. From where do cytokines come from?
Lymphocytes
secondary
Activate macrophages
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

14. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
Wiskott Aldrich syndrome
Secretory component
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

15. What is muromonab - CD3 (OKT3)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Popliteal
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

16. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Immunoflourescent staining of tissue biopsies
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
dimer
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!

17. other than eat and bite RBCs what else do Macrophages of spleen do>
Anemias (esp due to renal failure)
Remove encapsulated bacateria
Steroid responsive nephrotic syndrome
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

18. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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 :(
Anti alpha subunit 3 of collagen on type IV bm
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

19. 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).
Anti viral and anti tumor
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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!

20. 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)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
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
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin

21. What does IgA pick up from epithelial cells before being secreted?
Receiving preformed Antibodies
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
Secretory component
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

22. What is the main cytokine that activates eosinophils?
MS - hay fever - SLE - goodpastures
Interferon gamma; Th1
Immunosuppression after kidney transplantation
IL 5

23. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti SS- A (anti RO) and Anti SS- B
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

24. What is the toxicity of muromonab?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MHC class molecules bind to KIRS or CD94 to prevent killing
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
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

25. IgE has the ___________ in the serum
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
lowest concentration
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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

26. Name 5 ways Antibody diversity is generated?
Celiac
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
CD56

27. Other than stimulating fever - what else does IL 6 do?
IL 4
Superior mesenteric
Stimulate the liver to release acute phase reactants
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

28. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
active complement pathway
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
except hyperacute

29. What is the presentation of scid? treatment?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

30. 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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Immunosuppression after kidney transplantation
Carbohydrate

31. Which is the main antibody in the delayed or secondary response to an antigen?
The patient could become cyanotic in the OR!
Antidesmoglein
IgG
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. is IgM an opsonizer?
Negative!
MS - hay fever - SLE - goodpastures
Cyclosporine - OKT3
MHC II - B7

33. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
CD56
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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 :(
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

34. What are the autoantibodies for pernicious anemia?
When you select for which MHC it will have; take out the lymphs that self react
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anti IF
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

35. What are the autoantibodies for polymyositis and dermatomyositis?
Hereditary angioedema; PNH
Anti Jo -1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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

36. What is recomb gamma interferon used for?
Chronic granulomatous disease
carboxy terminal
Histamine; post capillary venules - vasodilation
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

37. describe the classic complement pathway.
Recom IL 11; thrombocytopenia
Anti glutamate carboxylase and anti insulin
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

38. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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

39. How does igA cross the epithelium?
The igA found in breast milk
By transcytosis
Negative nitroblue tetrazolium reduction test
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

40. What is three common causes of severe combined immunodef? What is the result of all three?
Hemochromatosis
IL 4 - 5 - 10 - 6
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Activate macrophages

41. Which disease is associated with B8?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
MHC I; from RER with help of the B2 microglobulin
Stimulate the liver to release acute phase reactants
Graves

42. hat is the presentation of Jobs syndrome or Hyper IgE?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Pernicious Anemia and Hashimotos
IgM and IgG

43. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
MHC I; from RER with help of the B2 microglobulin
except hyperacute
B - T - and NK cells
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

44. How do you test for chronic granulomatous disease?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Negative nitroblue tetrazolium reduction test
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
Anti mitochondrial

45. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
The igA found in breast milk
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Hereditary angioedema; PNH
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

46. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
Hereditary angioedema; PNH
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
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

47. What is the most common example of passive immunity?
IgAs in mothers breast milk!
TNF alpha and IL1
MS
Immunosuppression after kidney transplantation

48. What are the PALS?
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Cells that stil have weird parts of their membrane that macrophages usually bite off

49. What is epo used for?
Popliteal
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
A chemotactic factor for neutrophils
Anemias (esp due to renal failure)

50. What is the treatment of acute transplant rejection?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Cyclosporine - OKT3
In the germinal center of secondary follicles (In the paler center)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

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USMLE Step 1 Immunology

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