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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. How do you test for chronic granulomatous disease?
Kill them because they have CD16 on them that recognize the FcG portion
Negative nitroblue tetrazolium reduction test
cannot cross placenta
Hereditary angioedema; PNH

2. What does Interferon alpha and beta do? how?
IL 3; supports growth and differentiation of bone marrow stem cells
...
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

3. What bugs can actually infect the lymph node itself?
Immunosuppression after kidney transplantation
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Interferon gamma and IL 2
Remove encapsulated bacateria

4. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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)

5. What is the presentation of scid? treatment?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Interferon gamma; Th1
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

6. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Antimicrosomal and antithyroglobulin
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

7. IgE has the ___________ in the serum
lowest concentration
Negative!
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Anti SS- A (anti RO) and Anti SS- B

8. which of the transplant rejections is antibody mediated? why does it occur?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

9. What is a factor that is a predictor for a bad transplantation?
Interferon gamma and IL 2
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Viral neutralization of igM and IgG!

10. 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)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

11. Leukocyte adhesion defect presents with...
By transcytosis
neutrophilia!
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Anti SS- A (anti RO) and Anti SS- B

12. 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
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

13. which cytokine inhibits TH2 cells? secreted by who?
C5a
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Interferon gamma; Th1

14. what happens in a deficiency of C1 esterase inhibitor? DAF?
IgM and IgD
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
MS
Hereditary angioedema; PNH

15. The lymphocytes are ________ origin
Internal iliac
mesenchymal
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Its main effect is a defect in Ab opsonization for killing

16. What are the autoantibodies for polymyositis and dermatomyositis?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
type four
T cell precursor
Anti Jo -1

17. Describe the Mannose Lectin pathway
IgM and IgG
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

18. What are the PALS?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
CD21 on B cells (although there is T cell lymphocytosis in EBV)
TNF alpha and IL1

19. Which disease is associated with B8?
Graves
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Th cells fail to produce interferon gamma; a lot of IgE
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

20. What is the toxicity of muromonab?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
IL 5

21. what characterizes an arthus reaction?
SP infections
Graves
neutrophilia!
Edema and necrosis in that region

22. How does igA cross the epithelium?
By transcytosis
A j chain
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
pale central germinal centers

23. What are the autoantibodies for graves?
Anti TSh receptor
Complement activation (active in both)
Anti topoisomerase
Not thymus - BM

24. The alternative pathway is the only constutively...
pentamer
CRP - C3b - IgM
T cell activation; no with CD 4 or CD 8
active complement pathway

25. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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
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
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

26. What is recomb beta interferon used for?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
isotype
When you select for which MHC it will have; take out the lymphs that self react
MS

27. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Axillary
Immunoflourescent staining of tissue biopsies
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Paracortex; viral infection

28. What are the autoantibodies for Mixed connective tissue disease?
Superficial inguinal
Anti U1 RNP (ribonucleoprotein)
MHC class molecules bind to KIRS or CD94 to prevent killing
IgA

29. What is recomb alpha interferon used for?
except hyperacute
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anti IF

30. What cytokines are released by Th1 cells?
Fab portion
Interferon gamma and IL 2
Anti Ach receptor
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

31. What does IL 2 do?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
acute phase reactants
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Activates cytotoxic CD 8 T cells as second signal

32. What lymph node drains the thigh?
Superficial inguinal
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
False! B cell class switching requires a second signal
S. aureus - E. Coli - aspergillus

33. What are the autoantibodies for goodpastures syndrome?
Superficial inguinal
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Anti alpha subunit 3 of collagen on type IV bm

34. In thymic development - What is the positive selection? negative selections?
When you select for which MHC it will have; take out the lymphs that self react
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

35. What is anergy? why does this occur?
Fc
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Increases expression of MHC I and MHC II and also activates NK cells

36. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
cannot cross placenta
Histamine; post capillary venules - vasodilation
Superior mesenteric

37. Describe complement dependent Type II hypersensitivity. Give an example.
DM type I
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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

38. What are the autoantibodies for pernicious anemia?
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
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
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
Anti IF

39. What is the autoantibody for SLE that is nonspecific? Specific?
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 :(
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
cannot cross placenta

40. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
T cell activation; no with CD 4 or CD 8
Its main effect is a defect in Ab opsonization for killing
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Immunosuppression after kidney transplantation

41. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
opsonizes
Influenza; antigenic shift; antigenic drift

42. Which disease is associated with DR3?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Lymphocytes
DM type I
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

43. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
pathogenesis
Pernicious Anemia and Hashimotos

44. What is the clinical use of Muromonab?
Antihistone
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Immunosuppression after kidney transplantation

45. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
IgE; by activating eosinophils
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Paracortex; viral infection

46. To what portion of the Antibody do the complements bind?
Fc
pathogenesis
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IgM and IgG

47. What is the clinical use for azathioprine?
Hemochromatosis
IgG
...
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

48. Which MHC presents intracellular peptides? how so?
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Antimicrosomal and antithyroglobulin
MHC I; from RER with help of the B2 microglobulin

49. What kinds of receptors activate innate immunity?
Superficial inguinal
TLR ad nuclear receptors
Antimicrosomal and antithyroglobulin
Superior mesenteric

50. In general What are T cells good for?
Histamine; post capillary venules - vasodilation
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Active; passive - fast but short half life (3 weeks!)
Anti viral and anti tumor