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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. What are the main symptoms of T cell immunodeficiencies?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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
Viral neutralization of igM and IgG!
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

2. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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 :(
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Active; passive - fast but short half life (3 weeks!)

3. What is the pathology in hyperacute transplant rejection?
Activates Th1 helper cells; Macrophages
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

4. What is the main function of TNF alpha? How does it do this?
If there is class switching and plasma cell production (that is when memory cells are produced)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Antimicrosomal and antithyroglobulin

5. What is the general structure of an Ab?
2 heavy chains and two light chains
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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

6. What is hereditary angioedema? What are the C3 levels?
Increases expression of MHC I and MHC II and also activates NK cells
Basophils! THey want IG E class switch!
Kill them because they have CD16 on them that recognize the FcG portion
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

7. What type of side chains are found on Fc region of an antibody?
A j chain
Axillary
Carbohydrate
Steroid responsive nephrotic syndrome

8. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
MHC I; from RER with help of the B2 microglobulin
Immunoflourescent staining of tissue biopsies
IgM and IgD

9. IgM can exist as a _______ also
Fab portion
pentamer
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
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. How is i Th1 helper cell inhibited?
No because no peptide fragment!
lowest concentration
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Cytokine IL 10 secreted by Th2

11. What lymph node drains the thigh?
Superficial inguinal
Cytokine IL 10 secreted by Th2
delayed!
MS

12. what cell surface proteins are on all APCs?
Delayed type hypersensitivity
MHC II - B7
Superficial inguinal
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

13. What cytokines are released by Th1 cells?
Antimicrosomal and antithyroglobulin
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Interferon gamma and IL 2
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

14. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
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
When you select for which MHC it will have; take out the lymphs that self react
Immunoflourescent staining of tissue biopsies
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

15. What are the main Cell surface proteins on T cells?
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

16. What is the white pulp of the spleen?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
pale central germinal centers
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Wiskott Aldrich syndrome

17. What does IL 10 do? who is secreted by?
secondary
Axillary
Anti viral and anti tumor
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

18. What is the clinical use for azathioprine?
secondary
...
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

19. What is digoxin immune Fab used for?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Antidote for digoxin intoxication
IgA
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

20. What is the presentation of Brutons agammaglobulinemia?
carboxy terminal
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Cytokine IL 10 secreted by Th2

21. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Hemochromatosis
Recom IL 11; thrombocytopenia
In the germinal center of secondary follicles (In the paler center)

22. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
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
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

23. What lymph node drains the duodenum - jejunum?
pentamer
Stimulate the liver to release acute phase reactants
Superior mesenteric
Superficial inguinal

24. What is the pathogenesis of a hypersensitivity reaction?
Kill them because they have CD16 on them that recognize the FcG portion
MHC I; from RER with help of the B2 microglobulin
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
Not thymus - BM

25. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Edema and necrosis in that region
pathogenesis
Anemias (esp due to renal failure)

26. What are the major functions of Antibodies?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
MS - hay fever - SLE - goodpastures
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

27. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Superior mesenteric
Acts as second signal on B cells to induce class switching to IgE and IgG
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
TNF alpha and IL1

28. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
pathogenesis
Graves
MS - hay fever - SLE - goodpastures

29. what mediates the type II hypersensitivity? What are the two different methods?
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
IgM and IgD
Antihistone
Antibody mediated cytotoxicity; either complement dependent or complement independent

30. What are the autoantibodies for polymyositis and dermatomyositis?
Anti Jo -1
IL 4 - 5 - 10 - 6
Axillary
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

31. Which antibody mediates immunity to worms? how?
IgM and IgA
IgE; by activating eosinophils
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
mesenchymal

32. What is filgrastim and sargramostim? and What is it used for?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
secondary
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

33. What is colostrum?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
The igA found in breast milk

34. IgE has the ___________ in the serum
Fab portion
lowest concentration
Remove encapsulated bacateria
A j chain

35. What are the autoantibodies for wegeners granulomatosis?
encapsulated
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

36. What is serum sickness? give an example.
Graves
Axillary
...
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

37. Which helper T cells' development is induced by IL 4? IL 12?
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
Th2; Th1
Negative selection
T cell activation; no with CD 4 or CD 8

38. What are the two signals to kill for NK cells?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
CRP - C3b - IgM
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

39. which interleukin receptor is required for NK development? activation?
IgE
IL 15; IL 12 - interferon Beta and interferon alpha
The igA found in breast milk
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

40. 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
IgG
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

41. Describe the Mannose Lectin pathway
Activates cytotoxic CD 8 T cells as second signal
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
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

42. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
IgE
Negative!
Alternative splicing of mRNA

43. What are the main symptoms of B cell immunodeficiencies?
SP infections
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Activate macrophages
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

44. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

45. How do you test for chronic granulomatous disease?
Negative nitroblue tetrazolium reduction test
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

46. What type of fenestrations are found in the red pulp of the spleen?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Barrel hoop basement membrane fenestrations
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

47. Describe complement dependent Type II hypersensitivity. Give an example.
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)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
Kill them because they have CD16 on them that recognize the FcG portion

48. The pathogenesis of contact dermatitis is ________ hypersensitivity
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
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
type four

49. what will NK cells do to cells covered in IgG Ab? why?
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
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Kill them because they have CD16 on them that recognize the FcG portion
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

50. What does granulysin do?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Inferior mesenteric
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Severe pyogenic infections early in life