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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. The alternative pathway is the only constutively...
Active; passive - fast but short half life (3 weeks!)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
active complement pathway
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

2. Which disease is associated with HLA A3?
Hemochromatosis
TGF beta and IL 10
When you select for which MHC it will have; take out the lymphs that self react
Cytokine IL 10 secreted by Th2

3. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
dimer
Hemochromatosis
Remove encapsulated bacateria

4. Type IV hypersensitivity is i...
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
not Ab mediated
Fab portion

5. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
MHC I - CD16 - CD56
Yes
Axillary

6. What is the treatment of acute transplant rejection?
T cell dysfunction
Negative selection
Cyclosporine - OKT3
Interferon gamma; Th1

7. What is an example of a parasite showing antigenic variation?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
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
Negative selection
except hyperacute

8. What are the major functions of Antibodies?
Activates cytotoxic CD 8 T cells as second signal
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anti topoisomerase

9. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
A - B - C; all the D's
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
IL 3; supports growth and differentiation of bone marrow stem cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

10. The lymphocytes are ________ origin
mesenchymal
CD56
2 heavy chains and two light chains
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. To what portion of the Antibody do the complements bind?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
RNA segment reassortment
Axillary
Fc

12. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
Immunoflourescent staining of tissue biopsies
T cell dysfunction

13. What does IL 4 do?
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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

14. what will NK cells do to cells covered in IgG Ab? why?
Kill them because they have CD16 on them that recognize the FcG portion
Its main effect is a defect in Ab opsonization for killing
Anti topoisomerase
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

15. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Antidesmoglein
Daclizumab; prevent ACUTE rejection of renal transplant
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
...

16. which antibody is involved in the primary response or immediate response to an antigen?
Anti viral and anti tumor
IgM
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

17. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
CRP - C3b - IgM
By transcytosis
Complement activation (active in both)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

18. What is the presentation of hyperIgM syndrome?
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
Severe pyogenic infections early in life
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Fc

19. which cytokine inhibits TH2 cells? secreted by who?
T cell precursor
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Interferon gamma; Th1
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

20. which antibodies prevent antigens from binding mucosal surfaces?
IgA
Alternative splicing of mRNA
If there is class switching and plasma cell production (that is when memory cells are produced)
CD21 on B cells (although there is T cell lymphocytosis in EBV)

21. What is the general structure of an Ab?
Humoral
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
2 heavy chains and two light chains
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

22. What bugs can actually infect the lymph node itself?
S. aureus - E. Coli - aspergillus
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
acute phase reactants
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

23. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
pathogenesis
Active; passive - fast but short half life (3 weeks!)

24. To what disease do the autoantibodies to IgG (rheumatoid factor)?
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Rheumatic arthritis

25. 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?
IL 15; IL 12 - interferon Beta and interferon alpha
If there is class switching and plasma cell production (that is when memory cells are produced)
not Ab mediated
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

26. What is the presentation of Brutons agammaglobulinemia?
mesenchymal
Graves
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

27. Which type of selection of thymic development provides central tolerance?
Negative selection
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
Popliteal
Superficial inguinal

28. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
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
Receiving preformed Antibodies
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

29. What are the autoantibodies for systemic sclerosis?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anti topoisomerase
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Chronic granulomatous disease

30. What is the toxicity of azathioprine?
...
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

31. ________ regulate the cell mediated response.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Humoral
IgG

32. How fast does it occur?
The patient could become cyanotic in the OR!
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
Axillary
C5a

33. 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
Kill them because they have CD16 on them that recognize the FcG portion
Graves
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

34. where do somatic hypermutation and class switching occur?
IgAs in mothers breast milk!
In the germinal center of secondary follicles (In the paler center)
Severe pyogenic infections early in life
By transcytosis

35. What is hereditary angioedema? What are the C3 levels?
Hemochromatosis
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
Anti SS- A (anti RO) and Anti SS- B
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

36. What are the autoantibodies for pemphigus bulgaris?
Tetanus - Botulinum - HBV - Rabies
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
2 heavy chains and two light chains
Antidesmoglein

37. What are the two signals required for Th1 cells? what happens after then activated?
cannot cross placenta
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
In the germinal center of secondary follicles (In the paler center)
T cell activation; no with CD 4 or CD 8

38. What is the clinical use for azathioprine?
Anti TSh receptor
Recom IL 11; thrombocytopenia
...
A j chain

39. What are four results of a splenectomy?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
T cell precursor
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

40. Other than stimulating fever - what else does IL 6 do?
Stimulate the liver to release acute phase reactants
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
pale central germinal centers

41. Which diseases are associated with DR4?
DM type I and RA
Humoral
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Histamine; post capillary venules - vasodilation

42. How does igA cross the epithelium?
T cell activation; no with CD 4 or CD 8
MHC I; from RER with help of the B2 microglobulin
By transcytosis
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

43. What does it mean if there are igM in the serum at birth?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
heavy chains
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

44. Type Iv hypersensitivity is...
delayed!
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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
MHC I - CD16 - CD56

45. From where do cytokines come from?
Active; passive - fast but short half life (3 weeks!)
Lymphocytes
Histamine; post capillary venules - vasodilation
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

46. hat is the presentation of Jobs syndrome or Hyper IgE?
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
Superior mesenteric
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
TNF alpha and IL1

47. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Macrophages - Dendritic cells - B cells
S. aureus - E. Coli - aspergillus
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

48. What does IgA pick up from epithelial cells before being secreted?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
IL 1 and IL 6
Antihistone
Secretory component

49. IgG...
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
RNA segment reassortment
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
opsonizes

50. what bacteria are a splenectomy patient most susceptible to? why?
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)
SP infections
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
Superficial inguinal