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KN-Pathology Block 2 > Robbins Immunopathology Ch 4 > Flashcards

Robbins Immunopathology Ch 4 Flashcards

1
Q

What is amyloidosis?

A

disease characterized by the abnormal extracellular deposition of certain proteins

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2
Q

T or F: One of the main functions of T cells is to recognize free circulating antigens in the blood?

A

False. T cells only recognize MHC bound antigens, not free floaters

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3
Q

What is TCR composed of?

A

alpha and beta chains as well as variable regions.

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4
Q

What will happen if CD3 is missing or defective?

A

T cells cannot be activated. AND ??

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5
Q

What receptor does the Epstein-Barr virus use to enter B cells?

A

CD21, which is a B cell receptor that recognizes complement breakdown products deposited on microbes and then promotes B cell response.

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6
Q

What are Langerhans cells?

A

dendritic cells of the epidermis.

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7
Q

What are plasmacytoid dendritic cells?

A

DCs that resemble plasma cells and are present in the blood and lympoid organs. They are major sources of the antiviral cytokine type I IFN.

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8
Q

Which Ab do FDCs bind to?

A

They have receptors for the Fc tails of IgG molecules and for complememnt proteins, using them to effectively trap antigens bound to antibodies and complement for presentation to B cells in lymohoid follicles.

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9
Q

Do FCDs present antigen to B cells? To T cells?

A

Yes they trap and antigens for presentation to B cells in secondary lymhoid tissue, BUT they do NOT present to T cells.

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10
Q

What cytokine do NK cells produce after encountering infected cells?

A

IFN-gamma

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11
Q

Which type of T helper cell will activate eosinophils? Which type will activate macrophages?

A

TH2 cells activate eosinophils

TH1 cells activate macros and other phagocytes

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12
Q

What are the costimulators for T cells?

A

B7 (CD80 and CD86), which are recognized by CD28 on the T cells.

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13
Q

Which cytokines are involved in inflammation?

A

TNF, IL-1, IL-6, IL-12, IL-23, and IFN-gamma

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14
Q

Which cytokines regulate lymphocyte responses and effector functions in adaptive immunity?

A

IL-2 and IL-4 are proliferation and differentiation of lymphocytes
IFN-gamma activates macrophages
IL-5 activates eosinophils

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15
Q

Which cytokine activates eosinophils?

A

IL-5

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16
Q

What are colony-stimulating factors?

A

cytokines that stimulate hematopoiesis and function to increase the output of leukocytes form the bone marrow

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17
Q

What is usually the first cytokine that CD4+ helper cells secrete and what does it do?

A

IL-2, which is a growth factor that acts on T lymphocytes to stimulate their proliferation, leading to an increase in the number of antigen-specific lymphocytes.

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18
Q

What cytokine is secreted by TH2 cells to effet B cells and what does it do?

A

TH2 cells secrete IL-4 to stimulate B cells to differentiate into IgE-secreting plasma cells.

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19
Q

Which cytokines to TH2 cells release?

A

IL-4 to stimulate B cells to produce IgE.
IL-5 to activate eosinophils
IL-13 to activate mucosal epithelial cells to secrete mucous and activates macrophages

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20
Q

What cytokines do TH17 cells secrete?

A

IL-17 to recruit neutrophils and promote inflammation

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21
Q

Which receptor is crucial to T helper function in activating other cells?

A

CD40, which binds to CD40 receptor on B cells and macros

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22
Q

What cytokine will T cells secrete after binding to CD40 on macrophages?

A

IFN-gamma, which is a potent macrophage activator.

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23
Q

What are the four types of hypersensitivity reactions?

A

Type I - immediate hypersensitivity
Type II - antibody-mediated
Type III immune complex-mediated
Type IV - Cell-mediated

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24
Q

Describe the mechanism and clinical presentations of Type I hypersensitivities.

A 
Immediate hypersensitivity (allergy). Results from activation of TH2 which produce of IgE antibody causing the immediate release of vasoactive amines and other mast cell degranulators. This causes vascular dilation, edema, smooth muscle contraction, mucus, tissue injury and inflammation. 
Includes anaphylaxis, allergies, and asthma
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25
Describe the mechanism and clinical presentations of Type II hypersensitivities.
antibody-mediated. IgG, IgM, bind to host cells or fixed tissues. Phagocytosis or lysis of target cells is activated by complement or Fc receptors and recruits leukocytes. This causes phagocytosis and cell lysis, inflammaation, and possibly functional derangements without cell injury. Includes hemolytic anemia and goodpasture syndrome
26
Describe the mechanism and clinical presentations of Type III hypersensitivities.
immune complex-mediated. Deposition of antigen-antibody complexse leads to complement activation and recruitment of leukocytes by complment producets and Fc receptors, which releases enzymes and other toxic molecules. This causes inflammation and necrotizing vasculitis. Includes systemic lupus, glomerulonephritis, serum sicknes and Arthus reactions
27
Describe the mechanism and clinical presentations of Type IV hypersensitivities.
cell-mediated. Activated T lymphocytes (mainly TH1 and TH17) release cytokines which activate macros and cause inflam. There is also T-cell mediated cytotoxicity. This cauess perivascular cellular infiltrates, edema, granulomas, and cell destruction. Includes dermatitis, MS, type 1 diabetes, and tuberculosis.
28
Which T helper cell is directly involved in allergic responses? What cytokines does it secrete?
TH2, it actiavtes the B cells to produce IgE, which will then degranulate mast cells causing the immediate reaction. Secretes IL-4, IL-5, and IL-13. IL-4 stimulates B cell-->IgE production. IL-5 activates eosinophils IL-13 stimulates epithelial mucus secretion.
29
What is mast cell sensitization?
Mast cells that have antigen-specific IgE permanently bound to them are "sensitized" to react to the antigen.
30
What role does PGD2 play in allergic reactions?
it is an abundant mediator generated by the cyclooxygenase pathway in mast cells that causes intesnse bronchospasm as well as increased mucus secretion.
31
What do LTC4 and LTD4 do?
they are the most potent vasoactive and spasmogenic agents known.
32
Which secretion products are responsible for the immediate allergic reaction?
PGD2, LTC4, and LTD4. these are the newly synthesized lipid-mediators
33
Which secretory molecules are responsible for the late-phase allergic reaction?
cytokines IL-4, IL-5 and IL-13 from TH2 cells.
34
Which type of hypersensitivity reaction is systemic lupus?
Type III, immune-complex mediated
35
What factors determine whether immune complex formation leads to tissue deposition and disease?
Size - larger complexes are cleared quickly and usually harmless. Small ones more likely to deposit Valency of antigen Avidity of the antibody
36
What type of antibodies can cause Type III hypersensitivity reactions?
IgG and IgM because these are the ones that activate complement cascades and Fc receptors.
37
What is the main clinical sign of immune complex hypersensitivity?
necrotizing vasculitis. NEcrotic vessels take on a smudgy eosinophilic appearance called fibrinoid necrosis, caused by protein/complex deposition
38
What is the Arthus reaction?
area of tissue necrosis appears as a result of acute immune complex vasculitis. Immune complexes are formed and precipitate around area of antigen injection. This will trigger response and cause lesions to occur within 4-10 hours after injection.
39
What type of hypersensitivity reaction is MS?
multiple sclerosis is a type IV, T cell-mediated hypersensitivity where T cells are activated by protein antigens in myelin
40
What will IL-12 release by DCs encourage TH0 cells to differentiate into?
TH1.
41
What is DTH (delayed-type hypersensitivity)?
T cell-mediated reaction that develops in response to antigen challenge in a previously sensitized individual. It is delayed 12 to 48 hours, which is the time it takes for effector T cells to be recruited to the site of antigen challenge and secrete cytokines.
42
What is the tuberculin reaction?
a classic example of DTH, where 8-12 hours after an intracutaneous injection of M. tuberculosis, a person who has had previous exposure will elicit a reaction. Used to test for previous TB exposure.
43
How do CTLs kill targets?
perforin-granzyme system. When CTLs engage their targets that present MHC class I and antigen complex, perforin binds to plasma membrane of target cell and promotes entry of granzymes, which cleave cellular capsases to trigger apoptosis.
44
What is the mechanism of T cell-mediated hypersensitivity?
CD4+ T cells that are exposed to a protein antigen differentiate into TH1 and TH17 effector cells. The next time they are exposed to antigen, they release cytokines IFN-gamma and IL-17 to activate macrophages and recruit leukocytes, causing inflammation.
45
What is central tolerance?
Immature lymphocytes that recognize self antigens in the central lymphoid organs are kiled by apoptosis. Some self-reactive B cells will switch to antigens that are not self-reactive
46
What is peripheral tolerance?
cleans up the things that slip past central tolerance mechanisms. Examples are lack of costimulators from APCs, which requires infection of invasion. Suppression by releasing IL-10 and TGF-beta, which dampen other T cells and competitively block B7s on APCs. All this by FOXP3 transcription factor. If that is defective you get IPEX AND activation -induced cell death by Fas ligand
47
What factors can lead to a failure of self-tolerance and the development of autoimmunity?
1. inheritance of susceptibility genes | 2. infections and tissue alterations that may expose self-antigen and activate APCs and lymphocytes in the tissues.
48
What is systemic lupus erhtyematosus (SLE)?
multisystem autoimmune disease. Primarily a failure to maintain self-tolerance, leading to large numbers of autoantibodies. Causes malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis, renal disorder, neurologic disorder, hematologic disorder, immunologic disorder or abnormal antinuclear antibodies (ANAs).
49
Is SLE more common in men or women?
10x more common in women
50
What are ANAs?
antinuclear antibodies, that are directed against several nuclear antigens: 1. DNA 2. histoness 3. nonhistone proteins bound to RNA 4. nuleolar antigens Incidence increases with age and seen in up to 15% of people.
51
What is usually the most damaging mechanism of SLE?
immune complex deposition
52
WHat is Sjogren Syndrom?
inflammatory diseases that affects primarily the salivary ad lacrimal glands, causing dryness of the mouth and eyes. Believed to be an anutimmune T cell reaction against one or more self antigens in these glands or towards a virus that infects them
53
What is systemic sclerosis (SS)?
commonly called scleroderma. Is characterized by progressive fibrosis involving th eskin, gastrointestinal tract and other tissues. result of activation of fibroblasts by cytokines produced by T cells.
54
What is Mixed connective tissue disease?
a spectrium of pathologic processes in patients who present with clinical features suggestive of SLE, polymystosis or SSS. Have high titers of antibodies to an RNP antigen called U1RNP. Paucity of renal disease and a very good response to corticosteroids, suggesting favorable long-term prognosis.
55
What is polarteritis nodosa?
necrotizing inflammation of the walls of blood vessels caused by deposition of immune complexes.
56
What disease is associated with unusually high amount of IgG4 in serum?
IgG4-related disease, causes whole slew of inflammation and autoimmune issues systemically.
57
What is an allograft?
transplant of an organ from one individual to another of the same species.
58
What is the main cause of allograft rejection?
MHC molecules
59
What is the difference between direct and indirect recognition in allograft rejection?
direct - CD8+ T cells recognize the foreign MHC and receive stimulation to become CTLs which will kill the graft cells. Indirect - CD4 T cells recognize foreign MHC after they have been picked up and processed by host APCs. They secrete cytokines and antibodies against the graft.
60
What is hyperacute rejection?
special form of rejection occuring f pre-formed anti-donor antibodies are present in the circulation of host before transplantation. Causes immediate rejection (within minutes) of allograft and cause clotting and complmeent activation. Rarely happens now due to screening
61
What is X-linked Agammaglobulinemia (Bruton Disease)?
(XLA) is characterized by the failure of pre-B cells to differentiate into B cells and results in absence of antibodies in blood. Mutation in tyrosine kinase in pre-B cell receptor. More common in males. Normal T cell-mediated responses, absence of plasma cells and germinal centers underdeveloped.
62
What is common variable immunodeficiency?
umbrella term for group of disorders characterized by hypogammaglobulinemia, impaired humoral response, and susceptibility to infections. Usually normal number of mature B cells, absent plasma cells, deficient T cell help. Prone to autoimmune diseases.
63
What is isolated IgA deficiency?
most common primary immune deficiency disease. IgA is major Ig for protecting mucosal secretions in airways and GI tract. Block in terminal differentiation of IgA-secreting B cells. Normal levels of IgG and IgM. Susceptibility to diarhhea and respiratory infections
64
What is hyper IgM syndrome?
Patients produce normal IgM, but cannot produce IgG, IgA, or IgE. Defect in T cells prevents induction of class switching in B cells. Usually a problem in the CD40 receptors.
65
What is DiGeorge Syndrome?
Aka thymic hypoplasia. congenital defect in thymic development with deficient T cell maturation. No T cell-mediated immunity, but B cells and serum Ig levels usually unaffected.
66
What is SCID?
severe combined immunodeficiency. defects in both humoral and cell-mediated immunity
67
What is the most devastating cytokine to have a defect in?
IL-7. IL-7 is the growth factor for survival of both immature B and T cell precursors in primary lymphoid organs. Without it you develop SCID.
68
What are the two most common causes of SCID?
common gamma chain mutation AND ADA deficiency
69
What is ADA deficiency?
??
70
What is common gamma chain mutation?
??
71
What problems would you expect from a defect that took out TH17 response?
chronic fungal and bacterial skin infections.
72
What type of problems would you expect from a defect that took out TH1 responses?
infections of atypical mycobacteria and other intracellular infections.
73
What is wiskott-aldrich syndrome?
x-linked diseases characterized by thrombocytopenia and vulnerability to recurrent infections. Depletion of T lymphocytes and loss of cellular immunity.
74
What results from a C3 defect?
susceptibility to pyogenic bacterial infections.
75
What will defects in C1q, C2 and C4 cause?
increase risk of immune complex-mediated disease. No increased risk of infection.
76
What will defects in C5-C9 cause?
loss of MAC, and susceptibility to Neisseria
77
What will a defect in regulatory protein C1 cause?
uncontrolled C1 activation, causing angioedema and localized edema of skin and mucous membranes. (anaphylatoxins)
78
What is the main cellular target of HIV?
CD4 T cells, | note however that they infect macros, DCs, and many other immune cells as well.
79
What is amyloidosis?
Protein misfolding disorder. condition associated with several inherited and inflammatory disorders in which extracellular deposits of fibrillar proteins are responsible for tissue damage and functional compromise. (called amyloid for historical reasons even though it has nothing to do with starch)
80
What is the amyloid light chain protein (AL)?
produced by plasma cells, and is made up of Ig light chains. Results in Ig light chain aggregation
81
What is an AA (amyloid-associated) fibril?
unique non-Ig protein derived from serum alymoid-associated protein synthesized in liver. Pathology when SAA builds up because of mutation in breakdown enzymes.
82
What is AB amyloid?
foundoin cerebral lesions of Alzheimers. peptide that is the core of cerebral plaques and the amyloid deposits in cerebral blood vessels.
83
What is Transthyretin (TTR)?
normal serum protein that binds and transports thyroxine and retinol. misfolding causes aggregates, which lead to familial amyloid polyneuropathies
84
What is beta2-microglobulin?
component of MHC class I. High levels of this protein are present in patients with renal disease.

KN-Pathology Block 2 (10 decks)

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