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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 is the treatment of acute transplant rejection?
Carbohydrate
Anti topoisomerase
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Cyclosporine - OKT3

2. Which is the main antibody that provides passive immunity to infants?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
RNA segment reassortment
In the germinal center of secondary follicles (In the paler center)
IgG

3. How is i Th1 helper cell inhibited?
Cytokine IL 10 secreted by Th2
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Anti TSh receptor
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

4. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
Chronic granulomatous disease
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
S. aureus - E. Coli - aspergillus

5. Give three examples of bacteria that use antigenic variation and how.
S. aureus - E. Coli - aspergillus
Wiskott Aldrich syndrome
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

6. Monomer in circulation - ___ when secreted
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
dimer
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
Previous transfusion; pregnant woman whose fetus had paternal antigens

7. What does IL 5 do?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Hemochromatosis
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

8. In general What are T cells good for?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Anti viral and anti tumor
Increases expression of MHC I and MHC II and also activates NK cells
Anti alpha subunit 3 of collagen on type IV bm

9. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

10. Which disease is associated with HLA A3?
Thrombocytopenia
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Hemochromatosis
Internal iliac

11. So antibodies are the effectors for the humoral response. List some of their functions.
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

12. What are the main Cell surface proteins on T cells?
Graves
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IgG
Rheumatic arthritis

13. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
RNA segment reassortment
Cross link

14. Complements are...
Negative nitroblue tetrazolium reduction test
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
acute phase reactants
Stimulate the liver to release acute phase reactants

15. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
Humoral
Viral neutralization of igM and IgG!
Basophils! THey want IG E class switch!

16. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Interferon gamma and IL 2
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
type four
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

17. What cytokines to Th2 secrete?
IgG
Anti IF
IL 4 - 5 - 10 - 6
Severe pyogenic infections early in life

18. when can graft versus host disease? What is the result?
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
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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

19. What lymph node drains the sigmoid colon?
Inferior mesenteric
T cell dysfunction
IgE
Interferon gamma and IL 2

20. What are the two signals to kill for NK cells?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
IgAs in mothers breast milk!
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
isotype

21. other than eat and bite RBCs what else do Macrophages of spleen do>
Type IV
NK cells
Rheumatic arthritis
Remove encapsulated bacateria

22. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
dimer
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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)

23. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
IgAs in mothers breast milk!
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Anti IF

24. 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?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Activate macrophages
Para aortic
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

25. What are the autoantibodies for other vasculitides?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti mitochondrial
Superior mesenteric
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

26. What is the presentation of Brutons agammaglobulinemia?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Th2; Th1
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

27. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
secondary
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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
dimer

28. What do multimeric antibodies require for assembly?
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
A j chain
Secretory component

29. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
If there is class switching and plasma cell production (that is when memory cells are produced)
pale central germinal centers
Viral neutralization of igM and IgG!
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

30. From where do cytokines come from?
Lymphocytes
Antidesmoglein
Anti alpha subunit 3 of collagen on type IV bm
RNA segment reassortment

31. is IgM an opsonizer?
secondary
Negative!
Celiac
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

32. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
...
Rheumatic arthritis
Anti viral and anti tumor
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 :(

33. What does IL 2 do?
Antidesmoglein
Activates cytotoxic CD 8 T cells as second signal
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Anti mitochondrial

34. what mediates the type II hypersensitivity? What are the two different methods?
Anti glutamate carboxylase and anti insulin
Antibody mediated cytotoxicity; either complement dependent or complement independent
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
IL 4

35. where do NK cells develop?
Not thymus - BM
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

36. What is the marginal zone of the spleen? what happens there?
Activates Th1 helper cells; Macrophages
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
MHC I - CD16 - CD56
dimer

37. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Immunoflourescent staining of tissue biopsies
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
acute phase reactants

38. are Th cells involved in trapping of antigens of endotoxin/LPS?
No because no peptide fragment!
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Inferior mesenteric

39. What are the T cell functions?
Lymphocytes
Activates cytotoxic CD 8 T cells as second signal
Liver! (they are proteins circulating in the blood)
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

40. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
dimer
Activates cytotoxic CD 8 T cells as second signal
Anti Jo -1
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

41. What does IgA pick up from epithelial cells before being secreted?
MHC I; from RER with help of the B2 microglobulin
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Secretory component
By transcytosis

42. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
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
Type IV
pentamer
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

43. Other than stimulating fever - what else does IL 6 do?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Stimulate the liver to release acute phase reactants
MS
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)

44. What is the toxicity of muromonab?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Acts as second signal on B cells to induce class switching to IgE and IgG

45. Name the three opsonins
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
CRP - C3b - IgM
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Superficial inguinal

46. What is muromonab - CD3 (OKT3)
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 :(
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Acts as second signal on B cells to induce class switching to IgE and IgG
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

47. What lymph node drains the upper limb?
Axillary
DM type I
Rheumatic arthritis
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

48. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
pentamer
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

49. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
opsonizes

50. which B and T cell disorder presents with specifically low IgM?
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
Wiskott Aldrich syndrome
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Thrombocytopenia