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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 is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IgE; by activating eosinophils
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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

2. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Acts as second signal on B cells to induce class switching to IgE and IgG
Yes
Wiskott Aldrich syndrome
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

3. Which diseases are associated with DR5?
Fc
Pernicious Anemia and Hashimotos
pathogenesis
Inferior mesenteric

4. Give three examples of bacteria that use antigenic variation and how.
dimer
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Wiskott Aldrich syndrome

5. The lymphocytes are ________ origin
Histamine; post capillary venules - vasodilation
B - T - and NK cells
mesenchymal
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

6. what bacteria are a splenectomy patient most susceptible to? why?
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

7. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Cytokine IL 10 secreted by Th2
delayed!
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

8. what ensure that a memory response is generated?
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
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Yes

9. Which antibody mediates immunity to worms? how?
dimer
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
IgE; by activating eosinophils

10. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Influenza; antigenic shift; antigenic drift
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

11. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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
IL 4 - 5 - 10 - 6
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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 :(

12. What is the presentation of scid? treatment?
Activate macrophages
T
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Cells that stil have weird parts of their membrane that macrophages usually bite off

13. Which is the main antibody that provides passive immunity to infants?
IL 4
Axillary
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

14. What is recomb gamma interferon used for?
Chronic granulomatous disease
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
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

15. IgM can exist as a _______ also
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
No because no peptide fragment!
Axillary
pentamer

16. What is immune complex disease? give an example.
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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

17. What are the autoantibodies for graves?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Anti TSh receptor
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
IgG

18. which antibodies prevent antigens from binding mucosal surfaces?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Basophils! THey want IG E class switch!
IgA
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

19. what cell surface proteins are on all APCs?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Basophils! THey want IG E class switch!
Th cells fail to produce interferon gamma; a lot of IgE
MHC II - B7

20. What lymph node drains the rectum (above the pectinate line)?
Internal iliac
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
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Graves

21. describe the pathogenesis of delayed type IV hypersensitivity
encapsulated
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Viral neutralization of igM and IgG!
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)

22. What are the T cell functions?
IgM and IgG
IgM and IgA
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

23. What does interferon gamma do? What two type of cells does it attack mostly?
Remove encapsulated bacateria
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Interferon gamma and IL 2

24. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Superficial inguinal
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

25. T/F B cells do not require a second signal
Bind FcG for antibody dependent cellular cytotoxicity
Secretory component
False! B cell class switching requires a second signal
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

26. What are the autoantibodies for Celiac disease?
T cell activation; no with CD 4 or CD 8
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgM and IgA
No because no peptide fragment!

27. What is the pathogenesis of acute transplant rejection? When does it occur?
Negative nitroblue tetrazolium reduction test
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
False! B cell class switching requires a second signal

28. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
IgG

29. What lymph node drains the scrotum?
Cytokine IL 10 secreted by Th2
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Superficial inguinal

30. __________ are a part of the innate system.
Anti smooth muscle
Influenza; antigenic shift; antigenic drift
T
NK cells

31. What are the two signals required for B cell class switching? Which is the second signal?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti viral and anti tumor
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Previous transfusion; pregnant woman whose fetus had paternal antigens

32. what secretes IL 4?
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
Basophils! THey want IG E class switch!
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

33. Which is the most abundant antibody in blood?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IgG
Cytokine IL 10 secreted by Th2
Paracortex; viral infection

34. To what portion of the Antibody do the complements bind?
Fc
Type IV
Local infection/inflammation; infection of the ln itself; metastasis
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

35. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Barrel hoop basement membrane fenestrations
pale central germinal centers
neutrophilia!

36. What is the pathology of acute transplant rejection? is it reversible?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Basophils! THey want IG E class switch!
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

37. What are the autoantibodies for polymyositis and dermatomyositis?
B - T - and NK cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
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
Anti Jo -1

38. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Negative!
Para aortic
IL 4

39. What is the pathogenesis of a hypersensitivity reaction?
secondary
MHC I - CD16 - CD56
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
MS

40. What is an example of a parasite showing antigenic variation?
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 :(
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)

41. How does igA cross the epithelium?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
By transcytosis
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
delayed!

42. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
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
Steroid responsive nephrotic syndrome
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

43. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
Paracortex; viral infection
TLR ad nuclear receptors
Influenza; antigenic shift; antigenic drift

44. IgE has the ___________ in the serum
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
Its main effect is a defect in Ab opsonization for killing
lowest concentration
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi

45. Describe complement dependent Type II hypersensitivity. Give an example.
mesenchymal
...
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
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

46. Name two endogenous pyrogens
CRP - C3b - IgM
dimer
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IL 1 and IL 6

47. What is three common causes of severe combined immunodef? What is the result of all three?
NK cells
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

48. What are the autoantibodies for myasthenia gravis?
By transcytosis
lowest concentration
Anti Ach receptor
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

49. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
When you select for which MHC it will have; take out the lymphs that self react
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)

50. What is the main cytokine released by T cells? What does it do
Macrophages - Dendritic cells - B cells
T
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IL 3; supports growth and differentiation of bone marrow stem cells