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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. which interleukin receptor is required for NK development? activation?
not Ab mediated
IgAs in mothers breast milk!
IL 15; IL 12 - interferon Beta and interferon alpha
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

2. How does the alternative pathway lead to MAC activation?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
RNA segment reassortment
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

3. The two heavy chains of an antibody contribute to the...
Fab portion
Recom IL 11; thrombocytopenia
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

4. What is the mechanism for sirolimus? what else it known as?
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
CRP - C3b - IgM
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
TGF beta and IL 10

5. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti Jo -1
All MHC 1/CD8

6. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
IgE; by activating eosinophils
Superior mesenteric
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

7. What is the main function of IL 12? other than macrophages who else can release IL 12?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B 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

8. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
pale central germinal centers
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Paracortex; viral infection

9. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Cross link
cannot cross placenta
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

10. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Glycoproteins; HLA
RNA segment reassortment
Anemias (esp due to renal failure)
C5a

11. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Sinusitis - otitis media - pneumonia
Basophils! THey want IG E class switch!
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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

12. What is the marginal zone of the spleen? what happens there?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
T
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
Kill them because they have CD16 on them that recognize the FcG portion

13. 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
secondary
Antibody mediated cytotoxicity; either complement dependent or complement independent
T cell precursor

14. what mediates the type II hypersensitivity? What are the two different methods?
Anti U1 RNP (ribonucleoprotein)
Graves
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Antibody mediated cytotoxicity; either complement dependent or complement independent

15. What can cause a lymph node enlargement?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Local infection/inflammation; infection of the ln itself; metastasis
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Hereditary angioedema; PNH

16. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Cells that stil have weird parts of their membrane that macrophages usually bite off

17. What is the pathology of acute transplant rejection? is it reversible?
not Ab mediated
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

18. What is epo used for?
Hemochromatosis
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Anemias (esp due to renal failure)

19. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Liver! (they are proteins circulating in the blood)
RNA segment reassortment
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
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

20. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
opsonizes
lowest concentration
Its main effect is a defect in Ab opsonization for killing

21. How is sirolimus different from tacrolimus?
except hyperacute
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
CD56
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

22. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Macrophages - Dendritic cells - B cells
active complement pathway
Activates Th1 helper cells; Macrophages
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

23. which type of immunity is slow but long lasting? as opposed to...
Previous transfusion; pregnant woman whose fetus had paternal antigens
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Carbohydrate
Active; passive - fast but short half life (3 weeks!)

24. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Its main effect is a defect in Ab opsonization for killing
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
IL 15; IL 12 - interferon Beta and interferon alpha

25. From where do cytokines come from?
A chemotactic factor for neutrophils
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
Lymphocytes
IL 4 - 5 - 10 - 6

26. What are the autoantibodies for type I diabetes mellitus?
Para aortic
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Anti glutamate carboxylase and anti insulin
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

27. what bacteria are a splenectomy patient most susceptible to? why?
IL 1 and IL 6
Interferon gamma and IL 2
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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

28. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Antihistone
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Paracortex
Anti TSh receptor

29. __________ are a part of the innate system.
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
NK cells
C5a
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

30. Complements are...
except hyperacute
acute phase reactants
T
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

31. What are the main Cell surface proteins on T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Kill them because they have CD16 on them that recognize the FcG portion
2 heavy chains and two light chains
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

32. What are the autoantibodies for Celiac disease?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Hemochromatosis
Carbohydrate
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

33. What is the most common example of passive immunity?
IgAs in mothers breast milk!
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
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
Interferon gamma and IL 2

34. What does IL 2 do?
Th cells fail to produce interferon gamma; a lot of IgE
TNF alpha and IL1
Activates cytotoxic CD 8 T cells as second signal
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

35. So antibodies are the effectors for the humoral response. List some of their functions.
Cyclosporine - OKT3
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

36. What lymph node drains the duodenum - jejunum?
active complement pathway
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Macrophages - Dendritic cells - B cells
Superior mesenteric

37. What are the autoantibodies for myasthenia gravis?
Fab portion
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
Anti Ach receptor

38. what will NK cells do to cells covered in IgG Ab? why?
B - T - and NK cells
Kill them because they have CD16 on them that recognize the FcG portion
Anti alpha subunit 3 of collagen on type IV bm
Immunosuppression after kidney transplantation

39. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Acts as second signal on B cells to induce class switching to IgE and IgG
Active; passive - fast but short half life (3 weeks!)
Paracortex
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

40. What are the two signals to kill for NK cells?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IgA

41. what characterizes an arthus reaction?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Histamine; post capillary venules - vasodilation
Steroid responsive nephrotic syndrome
Edema and necrosis in that region

42. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Liver! (they are proteins circulating in the blood)
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
pentamer

43. The alternative pathway is the only constutively...
active complement pathway
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IL 1 and IL 6
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

44. Monomer in circulation - ___ when secreted
Chronic granulomatous disease
Cyclosporine - OKT3
dimer
T

45. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
TGF beta and IL 10
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a

46. What are the autoantibodies for other vasculitides?
Superficial inguinal
IL 5
IgM and IgD
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

47. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Interferon gamma and IL 2
TLR ad nuclear receptors

48. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Its a serine protease that activates apoptosis; NK and CD8
Rheumatic arthritis
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
Lymphocytes

49. What is the main function of IL 8?
MHC I - CD16 - CD56
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
SP infections
A chemotactic factor for neutrophils

50. To what portion of the Antibody do the complements bind?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
A j chain
Fc
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants