Test your basic knowledge |

USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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 the main function of interferons?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Receiving preformed Antibodies

2. What are the autoantibodies for drug induced lupus?
delayed!
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
TNF alpha and IL1
Antihistone

3. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
All MHC 1/CD8
isotype
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

4. Monomer in circulation - ___ when secreted
Antidote for digoxin intoxication
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
dimer

5. Which HLA's are included in MHC I? MHC II?

Warning: Invalid argument supplied for foreach() in /var/www/html/basicversity.com/show_quiz.php on line 183

6. What lymph node drains the stomach?
Daclizumab; prevent ACUTE rejection of renal transplant
RNA segment reassortment
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
Celiac

7. What are the autoantibodies for hashimotos?
carboxy terminal
Thrombocytopenia
Antimicrosomal and antithyroglobulin
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

8. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Stimulate the liver to release acute phase reactants
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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

9. Which is the most abundant antibody in blood?
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
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
IgG
When you select for which MHC it will have; take out the lymphs that self react

10. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Immunosuppression after kidney transplantation
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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

11. Which diseases are associated with DR4?
Delayed type hypersensitivity
DM type I and RA
Wiskott Aldrich syndrome
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

12. What is epo used for?
Anemias (esp due to renal failure)
NK cells
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection

13. In general What are T cells good for?
Pernicious Anemia and Hashimotos
Anti viral and anti tumor
A chemotactic factor for neutrophils
By transcytosis

14. What are the autoantibodies for type I diabetes mellitus?
Its main effect is a defect in Ab opsonization for killing
...
Anti glutamate carboxylase and anti insulin
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

15. The idiotype; the Fc portion determines the...
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
isotype

16. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
No because no peptide fragment!
Liver! (they are proteins circulating in the blood)

17. What is an example of a parasite showing antigenic variation?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

18. which antibody is involved in the primary response or immediate response to an antigen?
isotype
IL 4 - 5 - 10 - 6
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IgM

19. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
MS
Superficial inguinal
Antimicrosomal and antithyroglobulin

20. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
Anti mitochondrial
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

21. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Macrophages - Dendritic cells - B cells
Edema and necrosis in that region
A chemotactic factor for neutrophils

22. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Axillary
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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

23. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anti mitochondrial
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea

24. What lymph node drains the upper limb?
Axillary
Fc
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)

25. Which is the main antibody in the delayed or secondary response to an antigen?
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
carboxy terminal
IgG
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

26. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
acute phase reactants
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Its main effect is a defect in Ab opsonization for killing
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

27. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Activates Th1 helper cells; Macrophages
Negative!
MS - hay fever - SLE - goodpastures
Receiving preformed Antibodies

28. The pathogenesis of contact dermatitis is ________ hypersensitivity
type four
TLR ad nuclear receptors
Receiving preformed Antibodies
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

29. What happens in a secondary follicle?
MHC I; from RER with help of the B2 microglobulin
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

30. What does granzyme do? who secretes it?
opsonizes
Its a serine protease that activates apoptosis; NK and CD8
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

31. What does IgA pick up from epithelial cells before being secreted?
T cell activation; no with CD 4 or CD 8
B - T - and NK cells
Celiac
Secretory component

32. What is the treatment of acute transplant rejection?
Active; passive - fast but short half life (3 weeks!)
Hereditary angioedema; PNH
Thrombocytopenia
Cyclosporine - OKT3

33. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Alternative splicing of mRNA
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
The patient could become cyanotic in the OR!

34. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
except hyperacute
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
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

35. What is the clinical use for azathioprine?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
...
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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

36. The ______ in the BM are DN - the DP are in the cortex of thymus
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
T cell precursor
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!
Activate macrophages

37. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
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
Acts as second signal on B cells to induce class switching to IgE and IgG
Anti SS- A (anti RO) and Anti SS- B

38. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Paracortex
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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
Cells that stil have weird parts of their membrane that macrophages usually bite off

39. What is the pathology in hyperacute transplant rejection?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
C5a
Receiving preformed Antibodies

40. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Influenza; antigenic shift; antigenic drift
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Rheumatic arthritis

41. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
Sinusitis - otitis media - pneumonia
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
No because no peptide fragment!
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

42. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Para aortic
Influenza; antigenic shift; antigenic drift
IgG
The igA found in breast milk

43. describe the classic complement pathway.
Antibody mediated cytotoxicity; either complement dependent or complement independent
Anti alpha subunit 3 of collagen on type IV bm
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

44. What are the labs in brutons agammaglobulinemia?
heavy chains
MHC I - CD16 - CD56
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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

45. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
IgM and IgG
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!
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

46. What is filgrastim and sargramostim? and What is it used for?
pale central germinal centers
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
pentamer
opsonizes

47. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Local infection/inflammation; infection of the ln itself; metastasis
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

48. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
IgA
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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
All MHC 1/CD8

49. What is serum sickness? give an example.
Popliteal
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
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

50. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Graves
T cell dysfunction
IgG