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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 does IL 5 do?
Immunosuppression after kidney transplantation
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Acts as second signal on B cells to induce class switching to IgE and IgG
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

2. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
acute phase reactants
Daclizumab; prevent ACUTE rejection of renal transplant
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

3. What links the adaptive and innate immunity?
DM type I
cannot cross placenta
False! B cell class switching requires a second signal
Complement activation (active in both)

4. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Cytokine IL 10 secreted by Th2
Histamine; post capillary venules - vasodilation
Delayed type hypersensitivity

5. 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
A recomb cytokine of IL 2; RCC and metastatic melanoma
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Wiskott Aldrich syndrome

6. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
Cross link
MHC class molecules bind to KIRS or CD94 to prevent killing
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

7. Which is the main antibody that provides passive immunity to infants?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgG
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

8. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
IgM and IgD
Yes

9. The secondary follicles have __________; primary follicles are dense
IL 3; supports growth and differentiation of bone marrow stem cells
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
pale central germinal centers
except hyperacute

10. What is the pathology in hyperacute transplant rejection?
TGF beta and IL 10
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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

11. can igG cross the placenta?
IL 4
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Yes
Popliteal

12. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Negative!
T cell precursor
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

13. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

14. What is the main function of IL 8?
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
A chemotactic factor for neutrophils
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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

15. What is a factor that is a predictor for a bad transplantation?
Activates cytotoxic CD 8 T cells as second signal
IgG
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Th cells fail to produce interferon gamma; a lot of IgE

16. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
IL 4
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
Paracortex; viral infection

17. What lymph node drains the thigh?
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
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
Superficial inguinal
Antidesmoglein

18. Which is the most abundant antibody in blood?
IgG
Type IV
CD56
Cyclosporine - OKT3

19. What does IL 4 do?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Negative selection
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Acts as second signal on B cells to induce class switching to IgE and IgG

20. What is serum sickness? give an example.
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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

21. What is the clinical use for sirolimus? what should you combine it with?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Lymphocytes
IgM and IgA

22. What is hereditary angioedema? What are the C3 levels?
Antimicrosomal and antithyroglobulin
Immunoflourescent staining of tissue biopsies
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
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

23. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

24. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
opsonizes

25. What is Aldesleukin? What is it used for
A recomb cytokine of IL 2; RCC and metastatic melanoma
Activates cytotoxic CD 8 T cells as second signal
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Anti Jo -1

26. What is the presentation of common variable immunodef? and What are the labs?
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
except hyperacute
Anti U1 RNP (ribonucleoprotein)
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

27. Which is the main antibody in the delayed or secondary response to an antigen?
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
All MHC 1/CD8
IgG

28. What is the pathogenesis of acute transplant rejection? When does it occur?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
2 heavy chains and two light chains
MHC II - B7

29. What is the marginal zone of the spleen? what happens there?
False! B cell class switching requires a second signal
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
Axillary
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

30. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
pentamer
delayed!
Superior mesenteric

31. which B and T cell disorder presents with specifically low IgM?
Wiskott Aldrich syndrome
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

32. What portion of the lymph node is not well developed in DiGeorge Syndrome?
dimer
Anti alpha subunit 3 of collagen on type IV bm
Wiskott Aldrich syndrome
Paracortex

33. What cytokines to Th2 secrete?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IL 4 - 5 - 10 - 6
Edema and necrosis in that region
Daclizumab; prevent ACUTE rejection of renal transplant

34. Describe complement dependent Type II hypersensitivity. Give an example.
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
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
Histamine; post capillary venules - vasodilation
Internal iliac

35. Which disease is associated with DR3?
dimer
Daclizumab; prevent ACUTE rejection of renal transplant
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
DM type I

36. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Activate macrophages
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Wiskott Aldrich syndrome

37. What is filgrastim and sargramostim? and What is it used for?
NK cells
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

38. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Anti SS- A (anti RO) and Anti SS- B
Bind FcG for antibody dependent cellular cytotoxicity
Alternative splicing of mRNA
T cell activation; no with CD 4 or CD 8

39. What does interferon gamma do to be antiviral?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Stimulate the liver to release acute phase reactants
Increases expression of MHC I and MHC II and also activates NK cells
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

40. What are the autoantibodies for graves?
Anti TSh receptor
Stimulate the liver to release acute phase reactants
Liver! (they are proteins circulating in the blood)
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

41. Which helper T cells' development is induced by IL 4? IL 12?
No because no peptide fragment!
RNA segment reassortment
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
Th2; Th1

42. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
Secretory component

43. what characterizes an arthus reaction?
...
Sinusitis - otitis media - pneumonia
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Edema and necrosis in that region

44. Only the _______ contribute to the Fc region
Cyclosporine - OKT3
Axillary
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
heavy chains

45. The alternative pathway is the only constutively...
T cell activation; no with CD 4 or CD 8
Anti smooth muscle
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
active complement pathway

46. What is oprelevkin? and What is it used for?
Superficial inguinal
Recom IL 11; thrombocytopenia
MS - hay fever - SLE - goodpastures
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig

47. What are the two signals to kill for NK cells?
Active; passive - fast but short half life (3 weeks!)
IgG
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
DM type I

48. What does it mean if there are igM in the serum at birth?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Cytokine IL 10 secreted by Th2
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

49. Describe the Mannose Lectin pathway
IL 3; supports growth and differentiation of bone marrow stem cells
Previous transfusion; pregnant woman whose fetus had paternal antigens
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
Activate macrophages

50. is IgM an opsonizer?
IgG
Negative!
CD21 on B cells (although there is T cell lymphocytosis in EBV)
CRP - C3b - IgM