Lecture 17+18+DLA Flashcards
(37 cards)
lactoferrin
anti-microbial
iron-binding protein that competes with
pathogens for iron, an essential metabolite
C-reactive protein (CRP)
Acute-phase protein that binds to phosphocholine in bacteria membranes and function in opsonization.
It activates complement via the classic pathway
Mannose-binding lectin (MBL)
MBL recognizes carbohydrate patterns, found on bacteria, viruses, protozoa, and fungi, resulting in activation of the lectin pathway of the complement system
Serum amyloid A protein (SAP)
binds to bacterial cell wall lipopolysaccharide and serves as a receptor for phagocyte attachment.
Implicated in several chronic inflammatory diseases, such as amyloidosis, atherosclerosis, and rheumatoid arthritis
serum amyloid A protein
interferon
a small protein that is produced by certain WBC’s and virally infected cells
produced in response to viruses, RNA, immune products, and antigens
Interferon alpha and Interferon beta (Type I)
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
Interferon gamma (Type II)
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
granuloma
the bodies mechanism to deal with a substance that cannot be removed
infectious causes:
TB, leprosy, histoplasmosis, ect.
non-infectious causes: crohn’s disease
IFN (gamma) and granulomas
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
The complement system
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
The classical pathway
adaptive immunity
- C1 bind to Ag-Ab complex
- activated C1 cleaves C4 and C2
- formation of C3 convertase
- C3 and C5 are cleaved
- sequential binding of C5b, C6-C9
The alternate pathway
innate immunity
Spontaneous cleavage of C3 based on multiple
initiators
requires factors B and D
formation of a less stable C3 convertase
needs properdin
MBL pathway
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
MAC
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
role of C5b - C9
cell lysis
opsonization
C3b
role of C3a and C5a
INF
role of C3b, C5b-C9
viral neutralization
Inhibit C1
C1 inhibitor
classical pathway
Deficiency results in angioedema (hereditary or
acquired)
Prevent assembly of C3 convertase
CR1 (CD35)
MCP (CD46)
C4b binding protein
factor H
Accelerate decay of C3 convertase
DAF (CD55)
Block MAC
CD59 (protectin), S protein, clusterin
Inactivates anaphylatoxin C3a and C5a
Anaphylatoxin inactivator
