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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.
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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 cell surface proteins for Macrophages? which two are for opsonins?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Histamine; post capillary venules - vasodilation
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

2. What is three common causes of severe combined immunodef? What is the result of all three?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Tetanus - Botulinum - HBV - Rabies

3. Which are the only two antiinflammatory cytokines?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
TGF beta and IL 10

4. which type of immunity is slow but long lasting? as opposed to...
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Its a serine protease that activates apoptosis; NK and CD8
Active; passive - fast but short half life (3 weeks!)

5. Complements are...
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
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
acute phase reactants
Glycoproteins; HLA

6. What is a factor that is a predictor for a bad transplantation?
Kill them because they have CD16 on them that recognize the FcG portion
Anti Jo -1
Anti smooth muscle
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

7. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Antihistone
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
Anti Ach receptor

8. What is the pathology seen in chronic transplant rejection?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
In the germinal center of secondary follicles (In the paler center)
IgA

9. What is epo used for?
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Anemias (esp due to renal failure)
RNA segment reassortment

10. What are some catalase positive organisms?
Superficial inguinal
Secretory component
S. aureus - E. Coli - aspergillus
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

11. How does the alternative pathway lead to MAC activation?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

12. What are target cells?
Cytokine IL 10 secreted by Th2
Steroid responsive nephrotic syndrome
Cells that stil have weird parts of their membrane that macrophages usually bite off
Remove encapsulated bacateria

13. where do NK cells develop?
Axillary
Kill them because they have CD16 on them that recognize the FcG portion
Secretory component
Not thymus - BM

14. IgE has the ___________ in the serum
mesenchymal
lowest concentration
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
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

15. What are the three types of APCs?
IL 4 - 5 - 10 - 6
Delayed type hypersensitivity
Macrophages - Dendritic cells - B cells
Paracortex

16. 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
Anti SS- A (anti RO) and Anti SS- B
2 heavy chains and two light chains
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

17. Type Iv hypersensitivity is...
Yes
Superior mesenteric
Anti TSh receptor
delayed!

18. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
IgG
Anemias (esp due to renal failure)
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

19. What does IL 2 do?
DM type I and RA
Anti Jo -1
Activates cytotoxic CD 8 T cells as second signal
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

20. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
T cell precursor
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Its a serine protease that activates apoptosis; NK and CD8
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

21. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
...
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

22. which antibodies can bind complement?
IgG
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
IgM and IgG
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

23. What are the main Cell surface proteins on T cells?
TNF alpha and IL1
TLR ad nuclear receptors
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IgM and IgG

24. What is hereditary angioedema? What are the C3 levels?
...
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
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

25. What is the receptor for EBV? On what cells is that located?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

26. What type of fenestrations are found in the red pulp of the spleen?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Barrel hoop basement membrane fenestrations
Antidote for digoxin intoxication

27. which antibodies prevent antigens from binding mucosal surfaces?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IgA
Alternative splicing of mRNA
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

28. give an example of how influenza does a major antigenic shift.
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
RNA segment reassortment
TNF alpha and IL1
Thrombocytopenia

29. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
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
T cell activation; no with CD 4 or CD 8
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

30. What is Aldesleukin? What is it used for
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
A recomb cytokine of IL 2; RCC and metastatic melanoma
Negative nitroblue tetrazolium reduction test
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

31. Which diseases are associated with DR5?
If there is class switching and plasma cell production (that is when memory cells are produced)
Pernicious Anemia and Hashimotos
pale central germinal centers
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

32. T/F B cells do not require a second signal
MS - hay fever - SLE - goodpastures
Inferior mesenteric
Kill them because they have CD16 on them that recognize the FcG portion
False! B cell class switching requires a second signal

33. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Edema and necrosis in that region
MHC I; from RER with help of the B2 microglobulin
IgE
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

34. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Lymphocytes

35. What can cause a lymph node enlargement?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anti mitochondrial
Local infection/inflammation; infection of the ln itself; metastasis
Interferon gamma and IL 2

36. what characterizes an arthus reaction?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Basophils! THey want IG E class switch!
Edema and necrosis in that region

37. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
2 heavy chains and two light chains
MHC I; from RER with help of the B2 microglobulin
Cross link
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

38. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Remove encapsulated bacateria
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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

39. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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 smooth muscle
IL 4

40. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Negative nitroblue tetrazolium reduction test
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IL 15; IL 12 - interferon Beta and interferon alpha

41. What is the toxicity of muromonab?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
T cell precursor
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

42. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
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
T cell precursor
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

43. IgM can fix complement but...
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Histamine; post capillary venules - vasodilation
cannot cross placenta

44. which interleukin receptor is required for NK development? activation?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
CRP - C3b - IgM
IL 15; IL 12 - interferon Beta and interferon alpha
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

45. other than C3a - what other complement acts as an anaphyloxin?
SP infections
C5a
Anti U1 RNP (ribonucleoprotein)
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

46. 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)
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MHC I; from RER with help of the B2 microglobulin
Anti IF

47. What are the symptoms of serum sickness?
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Severe pyogenic infections early in life

48. What are the T cell functions?
...
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Superficial inguinal
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

49. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Immunosuppression after kidney transplantation

50. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Hereditary angioedema; PNH
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
Tetanus - Botulinum - HBV - Rabies