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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. 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).
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
Para aortic
Influenza; antigenic shift; antigenic drift
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!

2. what will NK cells do to cells covered in IgG Ab? why?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
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)
Kill them because they have CD16 on them that recognize the FcG portion

3. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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
Anti U1 RNP (ribonucleoprotein)
Fab portion

4. Describe complement dependent Type II hypersensitivity. Give an example.
Kill them because they have CD16 on them that recognize the FcG portion
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Complement activation (active in both)
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

5. 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
Active; passive - fast but short half life (3 weeks!)
Activates Th1 helper cells; Macrophages
IgM and IgA

6. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Cells that stil have weird parts of their membrane that macrophages usually bite off
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
CRP - C3b - IgM

7. when can graft versus host disease? What is the result?
Rheumatic arthritis
Wiskott Aldrich syndrome
Antimicrosomal and antithyroglobulin
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

8. Which are the only two antiinflammatory cytokines?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
All MHC 1/CD8
TGF beta and IL 10
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

9. What is a factor that is a predictor for a bad transplantation?
delayed!
Complement activation (active in both)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

10. What is the clinical use for sirolimus? what should you combine it with?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
The patient could become cyanotic in the OR!
IgM and IgG

11. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Wiskott Aldrich syndrome
A - B - C; all the D's
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

12. What does IgA pick up from epithelial cells before being secreted?
IgE
Rheumatic arthritis
A - B - C; all the D's
Secretory component

13. How is the thymus organized? what happens in each section?
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
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
pentamer

14. What are the PALS?
heavy chains
IgG
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

15. give an example of how influenza does a major antigenic shift.
Previous transfusion; pregnant woman whose fetus had paternal antigens
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Immunosuppression after kidney transplantation
RNA segment reassortment

16. What are the symptoms of serum sickness?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
A recomb cytokine of IL 2; RCC and metastatic melanoma

17. Name two endogenous pyrogens
TNF alpha and IL1
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
IL 1 and IL 6
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

18. Only the _______ contribute to the Fc region
heavy 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
Humoral
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

19. A lymph node is a ________ lymphoid organ.
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
secondary
Immunoflourescent staining of tissue biopsies
Influenza; antigenic shift; antigenic drift

20. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Glycoproteins; HLA
Activates Th1 helper cells; Macrophages
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

21. How does complement link innate and adaptive?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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
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
Carbohydrate

22. what characterizes an arthus reaction?
cannot cross placenta
...
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
Edema and necrosis in that region

23. What is the main function of IL 8?
S. aureus - E. Coli - aspergillus
A chemotactic factor for neutrophils
Recom IL 11; thrombocytopenia
In the germinal center of secondary follicles (In the paler center)

24. Describe the Mannose Lectin pathway
IL 4
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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
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

25. What lymph node drains the stomach?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Fc
Viral neutralization of igM and IgG!
Celiac

26. Name 5 ways Antibody diversity is generated?
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
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
Cytokine IL 10 secreted by Th2
Thrombocytopenia

27. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
MHC class molecules bind to KIRS or CD94 to prevent killing
Paracortex; viral infection
Superficial inguinal
Receiving preformed Antibodies

28. How fast does it occur?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
The patient could become cyanotic in the OR!

29. 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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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)
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

30. What is epo used for?
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)
Anemias (esp due to renal failure)
pathogenesis
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

31. What are the autoantibodies for hashimotos?
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
Antimicrosomal and antithyroglobulin
Chronic granulomatous disease
Anti TSh receptor

32. What is thrombopoietin used for?
Thrombocytopenia
Anti viral and anti tumor
MS
When you select for which MHC it will have; take out the lymphs that self react

33. 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
Negative!
Internal iliac
Thrombocytopenia

34. What are the autoantibodies for graves?
Axillary
The patient could become cyanotic in the OR!
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Anti TSh receptor

35. What are the autoantibodies for pemphigus bulgaris?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Antidesmoglein
Humoral
carboxy terminal

36. What are the main symptoms of T cell immunodeficiencies?
Stimulate the liver to release acute phase reactants
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

37. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Interferon gamma; Th1
2 heavy chains and two light chains

38. What are the autoantibodies for type I diabetes mellitus?
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
Anti glutamate carboxylase and anti insulin
Negative selection
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

39. What is the defect in hyper IgM syndrome? What are the lab results?
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 the germinal center of secondary follicles (In the paler center)
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

40. The secondary follicles have __________; primary follicles are dense
Yes
pale central germinal centers
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
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

41. What is the presentation of Brutons agammaglobulinemia?
IgM and IgG
Axillary
Basophils! THey want IG E class switch!
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

42. From where do cytokines come from?
Lymphocytes
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
NK cells
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

43. What is three common causes of severe combined immunodef? What is the result of all three?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
except hyperacute

44. What is colostrum?
Anti mitochondrial
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
The igA found in breast milk
Activate macrophages

45. Complements are...
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
acute phase reactants
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Immunoflourescent staining of tissue biopsies

46. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
SP infections
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
MHC II - B7
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

47. What are the autoantibodies for polymyositis and dermatomyositis?
CD56
IgG
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
Anti Jo -1

48. which type of immunity is slow but long lasting? as opposed to...
Anti viral and anti tumor
Activate macrophages
Active; passive - fast but short half life (3 weeks!)
Anti glutamate carboxylase and anti insulin

49. What are the autoantibodies for goodpastures syndrome?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Anti alpha subunit 3 of collagen on type IV bm
Alternative splicing of mRNA
Lymphocytes

50. So antibodies are the effectors for the humoral response. List some of their functions.
Immunoflourescent staining of tissue biopsies
The patient could become cyanotic in the OR!
Anti viral and anti tumor
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization