Immunology USMLE

Frage	Antworten
Secretes interleukin (IL-1) to promote T cell activity	Macrophage
Expresses high levels of major histocompatibility complex (MHC) class 2 on its cell membrane	Macrophage
Macrophage precursor	Monocyte
Total levels and concentration of this antibody can be estimated using radioimmunoabsorbent test (RIST) and radioallergosorbent test (RAST)	IgE
What term is used to describe the portion of a molecule that serves as an antigen determinant?	Epitope
Type 1 reactions involve both primary and secondary mediators. Explain the difference between the two	Primary mediators: preformed molecules stored in granules that are directly released. Secondary mediators: generated de novo as a consequence of mast cell/basophil activation.
Histamine and proteases/hydrolases are primary mediators. What are their functions?	Histamine: vasodilation, increases vascular permeability and plasma leak (edema formation), smooth muscle contraction increases secretions (nasal, respiratory) Proteases/hydrolases: tissue damage, activate complement, cleavage of membrane receptors.
Leukotrienes B4, C4, D4, and E4 and cytokines are secondary mediators. What are their functions?	Leukotrienes: B4 -> recruits white blood cell (WBC). C4/D4/T4 -> vasodilation, increases vascular permeability. Cytokines: mediate the inflammatory response of the late phase
What are the two phases of type I hypersensitivity reactions?	Immediate phase: rapid degranulation of performed mediators in mast cells/basophils within minutes of reexposure to antigen that cross-links the cell-bound IgE. Late phase: 2 to 48 hours after antigen exposure; secondary mediators cause an influx, maturation and activation of inflammatory cells and increase their survival in tissue.
What are the symptoms of the immediate phase of type 1 reactions?	Edema, erythema, wheal and flare reaction in the skin, itching (skin, eye, nose), runny nose, wheezing.
What are the symptoms of the late phase of type I reactions?	Edema and induration (firmness due to increased tissue density), wheezing
What are the common clinical manifestations of type I hypersensitivity reactions?	Skin: urticarcia (hives), eczema Airways: rhinitis, asthma Eyes: Conjunctivitis
What are the consequences of IgE mediated responses in the gastrointestinal (GI) tract, airways and blood vessels?	GI tract: Increased fluid secretion, increased peristalsis -> expulsion of GI tract contents (diarrhea, vomitting) Airways: decreased diameter, increased mucus secretion -> expulsion of contents (phlegm, coughing) Blood vessels: increased blood flow, increased permeability -> edema, inflammation, and increased lymph flow takes antigen to lymph nodes
What is the most severe form of type I hypersensitivity reactions?	Systemic anaphylaxis, which manifests as life-threatening bronchoconstriction and systemic vasodilation (eg hypotensive shock)
What are some common cause of anaphylaxis	Peanut, bee venom, drug and latex allergy
What drugs are commonly given to prevent anaphylactic reactions?	Antihistamines, corticosteroids, and cromolyn sodium. Epinephrine can be given as treatment for anaphylactic reactions
How does cromolyn sodium work on mast cells?	It stabilizes mast cell membranes preventing degranulation
What do patients with atopic disorders (asthma, eczema and urticarcia) have elevated levels of?	IgE, Th2 cytokines
Drugs commonly cause hypersensitivity reactions by acting as haptens. What is a hapten and how does this induce hypersensitivity reactions?	A hapten is a molecule, which by itself cannot induce an immune response. The hapten, usually a drug of its metabolite, binds to an endogenous protein that then induces antibody formation. The antibody reacts to the hapten (drug or its metabolite) upon subsequent exposure.
What are type 2 hypersensitivity reactions also known as?	Cytotoxic hypersensitivity
What reaction occurs in type 2 hypersensitivity?	Antibodies against endogenous ell membrane antigens fix complement causing complement mediated lysis via membrane attack complex
For each disease associated with type 2 hypersensitivity, name the target:	.
Warm/cold autoimmune hemolytic anemia	Self-RBC membrane proteins (warm IgG, cold IgM)
Erythroblastosis fetalis	Fetal D-Rh antigen
Pernicious anemia	Intrinsic factor (binds B12)
Antineutrophil cytoplasmic antibodies (ANCA) vasculitis	Neutrophil granule proteins
C-Anca	PR3
P-ANCA	Myeloperoxidase
Goodpasture syndrome	Alveolar and glomerular basement membranes
Rheumatic fever	Myocardial antigens that cross-react with streptococcal antigens (possibly the Streptococcus M protein)
Graves disease	Thyroid-stimulating hormone (TSH) receptor
Myasthenia gravis	Acetylcholine receptor
Lambert-Eaton myasthenic syndrome	Presynaptic Ca2+ channels
Pemphigus vulgaris	Epidermal desmosomes
Bullous pemphigpoid	Epidermal-dermal hemi-desmosomes
What drugs are associated with warm autoimmune hemolytic anemia? Of these, which drug (s) are associated with haptens? Which drug (s) generate autoantibodies?	Penicillin and quinidine are hapten forming. a-Methyl dopa generates autoantibodies
What test is positive in warm autoantibody disease?	Direct antiglobulin (Coombs) test
Cold autoimmune hemolytic disease has an acute and chronic form. What infections are associated with the acute form? What type of neoplasm is associated with the chronic form?	Acute form is associated with Mycoplasma pneumoniae and infectious mononucleosis (Epstein-Barr virus). Chronic form is associated with lymphoid neoplasms.
How is autoantibody is Grave disease different from other autoantibodies?	The autoantibody in Grave disease, a thyroid-stimulating immunoglobulin (TSI), actually binds and activates the TSH receptor.
What type 2 disease is mediated by an autoantibody that shares the same target as exfoliatin (Staphylococcus toxin in scaled skin syndrome) ?	Pemphigus vulgaris
What region of the autoantibodies attaches to the antigen in type 2 reactions? What region binds the complement?	IgG or IgM attaches to the antigen at their Fab region and attaches complement at their Fc region.
What are type 3 hypersensitivity reactions also known as?	Immune complex hypersensitivity
In type 3 reaction, formation of large antigen-antibody immune complexes deposit into tissues and fix complement. How does activation of complement result in tissue damage? How does this differ from type 2 hypersensitivity?	Complement activation recruits neutrophils, which release proteolytic enzymes and cause tissue damage. This differs from type 2 hypersensitivity in which tissue damage is caused by autoantibody-mediated complement activation (not by formation of large immune complexes)
One important factor that determines if antigen-antibody complexes deposit into tissue is the relative amount of antigen versus antibody. Why do antigen-predominant complexes typically form pathogenic deposits?	Antigen-antibody complexes are cleared when mononuclear phagocytes bind to antibody, resulting in endocytosis of the complex. In antigen-predominant complexes, fewer antibodies means less clearance and a propensity to form pathogenic deposits.
What is a pathology term used to describe type 3 inflammation in vessels?	Fibrinoid necrosis (eosinophilic staining accumulation)
What are the two typical type 3 hypersensitivity reactions?	1) Arthus reaction: local deposition of immune complexes 2. Serum sickness: systemic inflammatory response to immune complexes deposits throughout the body.
Describe how an Arthus reaction is evoked:	Antigen is subcutaneously injected into a host with preformed antibodies to this antigen causing local edema and possible ulceration.
Hypersensitivity pneumonitis (farmer lung) is an Arthus reaction caused by inhalation of what bacteria?	Thermophilic actinomycetes
What is the typical clinical presentation of serum sickness?	Fever, hives, arthralgia, lymphadenopathy, splenomegaly and eosinophilia appear days to weeks after antigen exposure.
What drug is associated with serum sickness?	Penicillin. Note that penicillin can cause type I, II and III via hapten formation.
What re well-known disease that are resulted from type 3 immune complex deposition?	Poststreptococcal glomeruloneprhitis, rheumatoid arthritis, and systemic lupus erythematosus.
What are type IV hypersensitivity reactions also known as?	Delayed type hypersensitivity
What are the two types of type IV hypersensitivity?	Classic (tuberculin-like) DTH Contact dermatitis
In the first step of classic dth, macrophages present antigens to CD4+ helper cells and induce CD4+ cells to become what specific subtype? What cytokine secreted by macrophages drives this process?	Macrophages induce CD4+ T cells to mature into Th1 cells. IL-12 is the cytokine that drives this process.
These Th1 cells often remains in the circulatory system as memory cells. When the body is exposed to the antigen for a subsequent time, what cells do these Th1 cells activate? What cytokine secreted by the Th1 cells drives this process?	Th1 cells activate macrophages. y-IFN is the cytokine that drives this process.
What functions are enhanced when a macrophage is activated?	Increased phagocytosis, increased antimicrobial potency, increased antigen presentation, and further induction of inflammation.
What is seen histopathologically in classic DTH?	Granuloma: central core of epithelioid cells (type of y-IFN activated macrophages) with a rim of lymphocytes
What pathogens trigger classic DTH?	Mycobacteria and fungi
A positive tuberculin skin test is a classic DTH. Describe how a positive test presents	Minimal change in the first few hours followed by erythema and in duration of 48 to 72 hours.
How does contact dermatitis differ from classic DTH?	In contact dermatitis, previously sensitized Th1 cells enter the dermis and cause cytokine-mediated cell necrosis as opposed to the granulomatous reactions seen in classic DTH.
What are common contact allergens?	Plants (poison ivy/oak), chemicals, soaps, jewelry metal, topical drugs.
What are the common symptoms of contact dermatitis?	Erythema, pruritus, and necrosis of skin with formation of large blisters within 24 hours.
What is the role of MHC class 2 proteins on donor cells in graft rejection?	Recognized by helper T cells of the host -> proliferation, cytokine production and help to activate cytotoxic T cells to kill the donor cells.
What are the immunological contraindications to organ transplantation?	ABO blood group incompatibility, presence of preformed human leukocyte antigen (HLA) antibodies in the recipient's serum.
What does a lymphocyte cross-match do?	Screens for recipient anti-HLA antibodies against donor lymphocytes
What are the typical mechanisms by which transplant recipients are presensitized to donor antigens	Pregnancy, previous transplantation, blood transfusion
The two types of immunity are innate and adaptive immunity. What cells mediate innate immunity?	Monocytes/macrophages, neutrophils, natural killer (NK) cells, gamma-delta T cells.
Adaptive immunity is composed of two responses. What cells mediate each response?	Humoral immunity is mediated by B lymphocytes. Cell mediated immunity is mediated by T lymphocytes (also macrophages, NK cells)
B and T cell proliferation in early lymphocyte maturation is stimulated by which cytokine?	Interleukin 7 (IL-7)
What interacts with the T-cell receptor (TCR) of an immature, double-positive T cell (CD4+/CD8+) to signal differentiation into a single positive cell? In what organ does this occur?	Interaction with either major histocompatibility complex 1 (MHC 1) (CD8+) or MHC2 (CD4+) in the cortex of the thymus
What two processes eliminate immature T cells lacking proper antigen receptor specificities?	Positive selection selects for lymphocytes with TCRs that recognize self-MHC proteins, ensuring that only T cells with TCR that recognize MHC mature 2. Negative selection eliminates autoreactive t cells that bind to MHC with high affinity.
What mechanism drives cell elimination in positive selection?	T cells that cannot bind to self-MHC molecules undergo apoptosis.
Apoptosis of T helper cells (CD4+, Th) or cytotoxic T cells (CD8+, Tc) bearing TCRs for self-proteins is the result of what process?	Tolerance, which prevents autoimmune reactions.
What cytokine released by activated Th further stimulates Th-cell survival/proliferation?	IL-2. It binds to the IL-2 receptor on Th cells causing further proliferation.
Name the two signals that are needed to activate T cells	The first signal is the MHC/antigen complex interaction with a TCR specific for that antigen. The second is costimulatory signal of the CD28 protein on the T cell with the B7 protein on the antigen-presenting cells (APCs)
What is the result of an interaction between a T cell and an APC in the absence of costimulation?	Anergy or unresponsiveness of T cells.
What T cell protein displaces CD28 from B7, inhibiting T cell activation and ensuring T cell homeostasis?	Cytotoxic T lymphocyte antigen 4 (CTLA-4)
What is a consequence to T cells that lack CTLA-4?	It is thought that cells without CTLA-4 participate more often in autoimmune processes.
Which MHC class molecule presents processed antigens from organisms that have been phagocytosed? What cells possess this MHC class?	MHC-2 complexes on professional APC present extracellular, phagocytosed proteins to Th cells.
What cells function as professional APCs?	Dendritic cells, macrophages and B cells.
What is the source of antigen presented by MHC-1 molecules? What cells possess this class?	MHC-1 complexes on all nucleated cells present intracellular proteins to the Tc cells.
What is the cluster of polypeptides present in all T cells that is important in signal transduction by the TCR?	The CD3 complex
Induction of which of the T-cell helper lines (Th1 or Th2) elicits a more effective response against intracellular pathogens such as Mycobacterium tuberculosis?	Th1 cells are more effective against intracellular pathogens.
Which cytokine released by Th1 cells is involved in macrophage activation?	y-Interferon
What other signaling pathway results in macrophage activation?	The interaction of CD40 on macrophages with CD40L on T cells.
What transcription factor is involved in both y-interferon and CD40/CD40L signaling?	Nuclear factor kB
How do macrophages respond to y-interferon and CD40/CD40L signalling?	Cytokine release, increased microbicidal activity, increased phagocytic activity (through upregulation of B7 and MHC 2)
Once activated, what are the major cytokines released by macrophages?	Tumor necrosis factor (TNF), IL-1 and IL-8, leukocyte recruitment, IL-6, lymphocyte activation and IL-12, Th1 differentiation.
What are the microbicidal substances produced by activated macrophages?	Reactive oxygen species, nitric oxide and lysosomal enzymes
Total levels and concentration of this antibody can be estimated using radioimmunosorbent test (RIST) and radioallergosorbent test (RAST)	IgE
What term is used to describe the portion of a molecule that serve as an antigenic determinant?	Epitope
What term is used to describe a small molecule that can serve as an antigenic determinant only if it is attached to a large carrier molecule?	Hapten

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