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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. How does complement link innate and adaptive?
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
Secretory component
When you select for which MHC it will have; take out the lymphs that self react
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

2. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Macrophages - Dendritic cells - B cells
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
A chemotactic factor for neutrophils

3. IgM can fix complement but...
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
cannot cross placenta
Hemochromatosis
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

4. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
cannot cross placenta
TNF alpha and IL1
Cells that stil have weird parts of their membrane that macrophages usually bite off
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

5. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
IgAs in mothers breast milk!
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Anti U1 RNP (ribonucleoprotein)

6. What type of side chains are found on Fc region of an antibody?
Carbohydrate
Activates Th1 helper cells; Macrophages
Active; passive - fast but short half life (3 weeks!)
A recomb cytokine of IL 2; RCC and metastatic melanoma

7. What are the cell surface proteins for Macrophages? which two are for opsonins?
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
IL 3; supports growth and differentiation of bone marrow stem cells

8. What is digoxin immune Fab used for?
Stimulate the liver to release acute phase reactants
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
Antidote for digoxin intoxication
Wiskott Aldrich syndrome

9. What are the two signals to kill for NK cells?
NK cells
Daclizumab; prevent ACUTE rejection of renal transplant
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

10. What is oprelevkin? and What is it used for?
Steroid responsive nephrotic syndrome
Delayed type hypersensitivity
Alternative splicing of mRNA
Recom IL 11; thrombocytopenia

11. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
If there is class switching and plasma cell production (that is when memory cells are produced)
T cell activation; no with CD 4 or CD 8
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

12. what cytokine does basophils secrete?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IL 4
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

13. What are the main symptoms of T cell immunodeficiencies?
Paracortex; viral infection
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Th2; Th1
No because no peptide fragment!

14. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
MS - hay fever - SLE - goodpastures
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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 the pathogenesis of HyperIgE syndrome? What are the labs?
pale central germinal centers
Anemias (esp due to renal failure)
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
Th cells fail to produce interferon gamma; a lot of IgE

16. How is sirolimus different from tacrolimus?
CD56
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Receiving preformed Antibodies
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

17. What is the white pulp of the spleen?
Glycoproteins; HLA
Its a serine protease that activates apoptosis; NK and CD8
Celiac
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

18. What lymph node drains the rectum (above the pectinate line)?
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
Antidesmoglein
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Internal iliac

19. what will NK cells do to cells covered in IgG Ab? why?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
Kill them because they have CD16 on them that recognize the FcG portion
S. aureus - E. Coli - aspergillus

20. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
pathogenesis
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

21. What is the main function of IL 8?
Antimicrosomal and antithyroglobulin
A chemotactic factor for neutrophils
pale central germinal centers
IgA

22. What are the two signals required for B cell class switching? Which is the second signal?
Cytokine IL 10 secreted by Th2
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Antihistone
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

23. IgG...
Macrophages - Dendritic cells - B cells
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
opsonizes
B - T - and NK cells

24. What are the autoantibodies for pernicious anemia?
Its a serine protease that activates apoptosis; NK and CD8
Anti IF
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Cyclosporine - OKT3

25. To what disease do the autoantibodies to IgG (rheumatoid factor)?
...
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Glycoproteins; HLA
Rheumatic arthritis

26. What does interferon gamma do? What two type of cells does it attack mostly?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

27. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
TLR ad nuclear receptors
Its main effect is a defect in Ab opsonization for killing
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

28. What links the adaptive and innate immunity?
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
Complement activation (active in both)
If there is class switching and plasma cell production (that is when memory cells are produced)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

29. where do NK cells develop?
Negative nitroblue tetrazolium reduction test
Activate macrophages
Superficial inguinal
Not thymus - BM

30. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Anti smooth muscle
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Antimicrosomal and antithyroglobulin
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

31. Type Iv hypersensitivity is...
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Th2; Th1
delayed!

32. What does granzyme do? who secretes it?
When you select for which MHC it will have; take out the lymphs that self react
Its a serine protease that activates apoptosis; NK and CD8
Liver! (they are proteins circulating in the blood)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

33. Which diseases are associated with DR2?
Antimicrosomal and antithyroglobulin
CD21 on B cells (although there is T cell lymphocytosis in EBV)
MS - hay fever - SLE - goodpastures
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

34. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Edema and necrosis in that region
Negative!
Antihistone

35. What cytokines to Th2 secrete?
Anti IF
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IL 4 - 5 - 10 - 6
T cell precursor

36. __________ are a part of the innate system.
IgM
Interferon gamma and IL 2
NK cells
Carbohydrate

37. What does IL 2 do?
Activates cytotoxic CD 8 T cells as second signal
Anti smooth muscle
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
Type IV

38. Which are the only two antiinflammatory cytokines?
All MHC 1/CD8
B - T - and NK cells
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
TGF beta and IL 10

39. The lymphocytes are ________ origin
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
mesenchymal
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

40. which B and T cell disorder presents with specifically low IgM?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Alternative splicing of mRNA
NK cells
Wiskott Aldrich syndrome

41. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Glycoproteins; HLA
IL 3; supports growth and differentiation of bone marrow stem cells
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

42. What is immune complex disease? give an example.
IgE; by activating eosinophils
Celiac
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

43. describe the pathogenesis of delayed type IV hypersensitivity
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Its main effect is a defect in Ab opsonization for killing
Active; passive - fast but short half life (3 weeks!)

44. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Superficial inguinal
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
MHC class molecules bind to KIRS or CD94 to prevent killing
CRP - C3b - IgM

45. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
carboxy terminal
Histamine; post capillary venules - vasodilation
IgE
Negative!

46. where are complements produced?
Lymphocytes
A j chain
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
Liver! (they are proteins circulating in the blood)

47. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Secretory component
Remove encapsulated bacateria
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
A - B - C; all the D's

48. What does interferon gamma do to be antiviral?
Anti Ach receptor
Increases expression of MHC I and MHC II and also activates NK cells
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
SP infections

49. What are the autoantibodies for myasthenia gravis?
Type IV
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Superior mesenteric
Anti Ach receptor

50. What lymph node drains the sigmoid colon?
T cell precursor
Antihistone
pentamer
Inferior mesenteric