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Exam 1 of term 3 > Lecture 17+18+DLA > Flashcards

Lecture 17+18+DLA Flashcards

1
Q

lactoferrin

A

anti-microbial

iron-binding protein that competes with
pathogens for iron, an essential metabolite

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2
Q

C-reactive protein (CRP)

A

Acute-phase protein that binds to phosphocholine in bacteria membranes and function in opsonization.

It activates complement via the classic pathway

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3
Q

Mannose-binding lectin (MBL)

A

MBL recognizes carbohydrate patterns, found on bacteria, viruses, protozoa, and fungi, resulting in activation of the lectin pathway of the complement system

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4
Q

Serum amyloid A protein (SAP)

A

binds to bacterial cell wall lipopolysaccharide and serves as a receptor for phagocyte attachment.

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5
Q

Implicated in several chronic inflammatory diseases, such as amyloidosis, atherosclerosis, and rheumatoid arthritis

A

serum amyloid A protein

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6
Q

interferon

A

a small protein that is produced by certain WBC’s and virally infected cells

produced in response to viruses, RNA, immune products, and antigens

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7
Q

Interferon alpha and Interferon beta (Type I)

A

Type I interferons can be produced by almost any cell upon stimulation by a virus

Act on neighboring uninfected cells

Inhibit transcription and translation of viral proteins

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8
Q

Interferon gamma (Type II)

A

Produced by: Th1, CTLs (CD8+), NK cells

promotes NK cell activity
increases the activity of macrophages

Activates inducible nitric oxide synthase (iNOS):
relaxes smooth muscle, vasodilation
induces the production of ab’s

normal cells will expresses MHC I + II after interaction

promoted adhesion and binding required for leukocyte migration

respond to cancer growth

will lead to the transcription of antiviral effects

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9
Q

granuloma

A

the bodies mechanism to deal with a substance that cannot be removed

infectious causes:
TB, leprosy, histoplasmosis, ect.

non-infectious causes: crohn’s disease

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10
Q

IFN (gamma) and granulomas

A

Association between IFNγ and granulomas: IFNγ
activates macrophages to kill intracellular organisms

activation of th1 helper cells by the macrophages
IL-1 and IL-12 by macrophages

Th1 helper cells aggregate around the macrophages

then IFN gamma activates the macrophages

macrophages surround the Th1 helper cells and
become fibroblast-like cells walling off the infection

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11
Q

The complement system

A

serum glycoproteins synthesized principally by hepatocytes, but also monocytes, macrophages, and epithelial cells

recruitment of inflammatory cells and the killing or opsonization of pathogens

Complement proteins are activated by cleavage (cascade reaction)
inactive precursors in blood: C2, C3, C4

C1 through C9

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12
Q

The classical pathway

A

adaptive immunity

  1. C1 bind to Ag-Ab complex
  2. activated C1 cleaves C4 and C2
  3. formation of C3 convertase
  4. C3 and C5 are cleaved
  5. sequential binding of C5b, C6-C9
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13
Q

The alternate pathway

A

innate immunity

Spontaneous cleavage of C3 based on multiple
initiators

requires factors B and D

formation of a less stable C3 convertase
needs properdin

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14
Q

MBL pathway

A

innate immunity

Mannan-binding lectin (MBL), an acute phase
protein found in serum binds to carbohydrate residues on cells or pathogen surfaces

MASP binds to MBL
MASP = MBL associated serine protein

this complex cleaves C4 and C2

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15
Q

MAC

A

the Three pathways converge with activation of C5
convertase

C5b binds antigenic surface
MAC is formed on surface

C5Components:
C5b,C6, C7, C8, C9

Poly -C9: perforin-like molecule

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16
Q

role of C5b - C9

A

cell lysis

17
Q

opsonization

A

C3b

18
Q

role of C3a and C5a

A

INF

19
Q

role of C3b, C5b-C9

A

viral neutralization

20
Q

Inhibit C1

A

C1 inhibitor

classical pathway

Deficiency results in angioedema (hereditary or
acquired)

21
Q

Prevent assembly of C3 convertase

A

CR1 (CD35)
MCP (CD46)
C4b binding protein
factor H

22
Q

Accelerate decay of C3 convertase

A

DAF (CD55)

23
Q

Block MAC

A

CD59 (protectin), S protein, clusterin

24
Q

Inactivates anaphylatoxin C3a and C5a

A

Anaphylatoxin inactivator

25
Q

Activator disorders: complement deficiency

A

under-reactive system. More susceptible to

infections

26
Q

inhibitor disorders: complement deficiency

A

overreactive system

27
Q

Classical pathway component deficiencies (C1, C4, C2)

A

more prone to immune complex disease
inability to clear circulating immune complexes
deposition into tissues

EX: Systemic Lupus Erythematosus (SLE),
Glomerulonephritis, Vasculitis

28
Q

MBL deficiency

A

Classically presents with recurrent pyogenic infection in childhood

Susceptibility to Saccharomyces cerevisiae, pneumococcal and Neisseria infections

can be auto dom or recessive

29
Q

Alternative pathway component deficiencies (Properdin, factor B and factor D)

A

Affected individuals are prone to pneumococcal and
meningococcal infections

Properdin deficiency: risk of overwhelming Neisseria infection

30
Q

C3 deficiency

A

C3 is required for opsonization

Primary C3 deficiency tends to present in early life with
overwhelming infection with encapsulated organisms

connective tissue diseases

31
Q

MAC deficiencies (C5-C9)

A

Recurrent infections

Common Infection with Neisseria meningitidis

32
Q

DAF (decay accelerating factor)/CD55 and CD59 deficiency

A

Paroxysmal Nocturnal Hemoglobinuria (lysis of red

blood cells)

33
Q

hereditary angioedema

A

characterized by episodic, nonpruritic, localized subcutaneous and submucosal swelling

dysregulation of three systems:
classic (C1), MLB (MASP-2)

excessive activation of the complement due to
mutation on C1inh results in high concentration
of anaphylatoxins: C3a and C5a

reduced C4 on testing

34
Q

The hemolytic titration (CH50) assay

A

needs all complement molecules in order to work

35
Q

prevalence formula

A

number of cases / size of the population

36
Q

point prevalence

A

of cases / # of persons

37
Q

incidence proportion

A

number of new cases of disease / pop. without the disease

Exam 1 of term 3 (15 decks)

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