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Innate Adaptive
Immediate Early induced Late
Pathogen
Physical PAMP, DAMP
barrier
(mucin, cilia) Recognition. TLR
Cell-mediated (T Humoral (B
APC (dendritic lymphocytes) Lymphocyte)
cells,
macrophage) Th2
T helper Plasma cells Clonal B
Recognition. TLR Th1 cells
Phagocytes Antibody
(macrophage, T cytotoxic Memory
Inflam
neutrophil),
basophil, mation
T
eosinophil, NK suppressor Complement
cascade
Complement Inflam
mation
Innate and adaptive immunity
Innate immunity
Innate immunity:
Happens early of infection
It consists of cellular and biochemical defense mechanisms
that are in place even before infection and are poised to
respond rapidly to infections.
1. Complement system
2. Collectins, pentraxins, and ficolins
3. Cytokines (TNF, IL1, IL6)
Complement nomenclature
The first proteins discovered belong to the classical pathway, and are
designated by the letter C followed by a number.
The native complement proteinssuch as the inactive zymogenshave a
simple number designation, for example C1 and C2.
The order of number is not sequence reaction but number of discovery. The
reaction sequence in the classical pathway, for example, is C1, C4, C2, C3, C5,
C6, C7, C8, and C9
Products of cleavage reactions are designated by adding a lowercase letter as
a suffix. For example, cleavage of C3 C3a (small) and C3b (bigger).
The larger fragment is always designated by the suffix b, except for C2 (C2a is
the larger fragment because it is the that enzymatically active fragment)
Another exception: naming of C1q, C1r, and C1s these are not cleavage
products of C1 but are distinct proteins that together comprise C1.
Alternative pathway naming are designated by different capital letters (e.g.
factor B and factor D). Activated complement components are sometimes
designated by a horizontal line, for example, C2a
Complements
Classical C1 (C1q: C1q Binds directly to pathogen surface or indirectly to Ab bound to pathogen,
C1r2:C1S thus allowing autoactivation of C1r
2
C1r Cleaves C1 to active protease
C1s Cleaves C4 and C2
C4 C4b Covalently binds to pathogen and opsonize it. Binds C2 for cleavage by C1s
C4a Peptide mediator of inflammation (weak)
C2 C2a Active enzyme of classical pathway C3/C5 convertase: cleaves C3 and C5
C2b Precursor of vasoactive C2 kinin
C3 C3b Many molecules of C3b bind to pathogen surface and act as opsonins.
Initiates amplification via alternative pathway. Binds C5 for cleavage by C2a
C3a Peptide mediator of inflammation (intermediate)
C3 C3b Binds to pathogen surface, binds B for cleavage by D, C3bBb is C3
Alternat
convertase and C3b2Bb is C5 convertase
ive
Factor B Ba Small fragment of B
Bb Bb is active enzyme of the C3 convertase C3bBb and C5 convertase C3b2Bb
Factor D D Plasma serine protease, cleaves B when it is bound to C3b to Ba and Bb
Properdin P Plasma protein that binds to bacterial surfaces and stabilizes the C3bBb
convertase
Pentraxins, Collectins, Ficollins
Pentraxins family: short pentraxins C-reactive protein (CRP), serum
amyloid P (SAP) and the long pentraxin PTX3 known as acute
phase reactants, because they content in plasma protein rise
during inflammation.
Microbe can
be directly
bound to
phagocyte
receptor or
opsonized
Antiviral response