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Immunology 2
- The complement system
- Innate
- Lectin Pathway: MBL (a recpetor)
binds to Mannose residues on the cell
surface of bacteria. The subsequent
MAPS-2 allows C3 convertase reaction
to occur
- Alternate pathway- In non infected cells
SALIC acid allows for the rapid destruction
of C3b which circulates in low levels. In
infected state the antigen will bind with
C3B as will Factor D, B and properidin to
form C3 Convertase
- The terminal pathway is the same for
all... The Anaphylotoxins (a)- C3a and
c5a will bind to MAST cells and
promote vasodilation. The c5b
activation is the patform of cascades
to form a polymer- The MAC attack
(membrane attack complex) product
allows for cell lesion/destruction
- The terminal pathway is the same for
all... The Anaphylotoxins (a)- C3a and
c5a will bind to MAST cells and
promote vasodilation. The c5b
activation is the patform of cascades
to form a polymer- The MAC attack
(membrane attack complex) product
allows for cell lesion/destruction
- Lectin Pathway: MBL (a recpetor)
binds to Mannose residues on the cell
surface of bacteria. The subsequent
MAPS-2 allows C3 convertase reaction
to occur
- Acquired
- The classial pathway:The is when a
single IGM or two adjacent IGG bind
to a C1 and alow subsequent c2-C4
cleavage to occu.The product is C3
CONVERTASE
- The classial pathway:The is when a
single IGM or two adjacent IGG bind
to a C1 and alow subsequent c2-C4
cleavage to occu.The product is C3
CONVERTASE
- A group of 25-30 proteins (lettered and
numbered) that are synthesized in the
LIVER. Membrane damage,immune
adherance and opsonization. This also
promotes chemotaxis and chemokines
- Innate
- Viral Infections
- Innate immunity: Anatomical,
Physiological, Phagocytic and
Inflammatory
- NK cells: These are cyttoxic to virally
infected cells, crucial in the first 1-2days.
They are able to recognise and destroy
"mutated MHC 1's"
- Interferons: These activate
neighbouring cells- they enhance the
acquired immune response via ^
expression of MHC 1/2
- NK cells: These are cyttoxic to virally
infected cells, crucial in the first 1-2days.
They are able to recognise and destroy
"mutated MHC 1's"
- Acquired Immunity
- Humoral *TH2: Theappropriae
release of cytokines allow for B
cell clonal selection. Production peaks 2-3 w after initial infection
- Antibodies do not break down cells,
they BLOCK the BINDING of the virus to
the HOST cell
- IgM, IgA and IgG
- IgM, IgA and IgG
- Opsonise for phagocytosis
- IgM and IgG
- IgM and IgG
- Agglutination of cells
- IgM (the primary response)
- IgM (the primary response)
- Antibodies do not break down cells,
they BLOCK the BINDING of the virus to
the HOST cell
- Cell Mediated Immunity *TH1:
- Cytotoxic T cells are MHC restricted but
they are able to lyse virally infected cells.
Macs are often the professional APC's to TH
cells and also aid in phagocytosis
- There are certain cytotinx
(IFN-gamma) which is released to
DIRECT antiviral activity
- NK cells can destroy via
ADCC and non specifically
- There are certain cytotinx
(IFN-gamma) which is released to
DIRECT antiviral activity
- Cytotoxic T cells are MHC restricted but
they are able to lyse virally infected cells.
Macs are often the professional APC's to TH
cells and also aid in phagocytosis
- Humoral *TH2: Theappropriae
release of cytokines allow for B
cell clonal selection. Production peaks 2-3 w after initial infection
- BOTH CMI and Humoral are key
- Innate immunity: Anatomical,
Physiological, Phagocytic and
Inflammatory
- Intracellular Bacteria
- The TH1- cyto0toxic response is the most important
- LISTERIA: This is a facultative anaerobe
that is widely distributed in the env. It may
penetrate the GIT and cause spleenic and
hepatic division. = Abortion, septicaemia
and meningitis
- Evades the immune system via
production of LYSIN, the lysosome is
destroyed- does not form and the
bacteria gains access to the cytoplasm.
After replication the pathogen travels to
the periphery (filaments) and enter
adjacent cells via membrane projections
(never exposed)
- Macs are activated- TNF is then released
which allows NK cells to produce IFN .
These macs also promote the direct
dstruction of infx hepatocytsThe release of
INTERFERON Y from NK cells is crucial to
supportive macrophage activation and
death of bacteria. Once the infection is
controlled, 1L-10 will down regulate the
response.
- Macs are activated- TNF is then released
which allows NK cells to produce IFN .
These macs also promote the direct
dstruction of infx hepatocytsThe release of
INTERFERON Y from NK cells is crucial to
supportive macrophage activation and
death of bacteria. Once the infection is
controlled, 1L-10 will down regulate the
response.
- Evades the immune system via
production of LYSIN, the lysosome is
destroyed- does not form and the
bacteria gains access to the cytoplasm.
After replication the pathogen travels to
the periphery (filaments) and enter
adjacent cells via membrane projections
(never exposed)
- There is activation of alveolar macs. These are
professional APC'S which activate TH cells,
release of interferon sways acquired immunity
predmoninantly towards CYTOTOXIC (TH1). A
primary tubercle attacked my macs is suported
by cytotoxic T cells
- These evade the immune system by hiding in
the "cornerstones" where they cannot be
attacked by" Macs, antibodies and the
Complement system. They are mobile and
rapid dissemination occurs. They PREVENT the
lysosome bind and bacteria can then escape
into the cytoplasm. They NOW produce a
"LETHAL HIT", necrosis and rapid spread
- Mycobacterium TB: A few pathogen enter the
bronchi (resp tract)
- Mycobacterium TB: A few pathogen enter the
bronchi (resp tract)
- A TUBERCLE forms in infected tissue (lungs, LN)-
calcified and radio-opaque. This is a combination
of macs and actuvated T cells. It is the site of
infection, protection, persistance and pathology.
It can become re-activated
- These evade the immune system by hiding in
the "cornerstones" where they cannot be
attacked by" Macs, antibodies and the
Complement system. They are mobile and
rapid dissemination occurs. They PREVENT the
lysosome bind and bacteria can then escape
into the cytoplasm. They NOW produce a
"LETHAL HIT", necrosis and rapid spread
- LISTERIA: This is a facultative anaerobe
that is widely distributed in the env. It may
penetrate the GIT and cause spleenic and
hepatic division. = Abortion, septicaemia
and meningitis
- The TH1- cyto0toxic response is the most important
- Extracellular Bacteria
- TH2 antibody productionis the main response but there are essentially
four methods... This icludes the CLOSTRIDIAL disease- Tetani, Boltulium,
Bacillus and ENTERObactericae- Yersninia, Klebsiella etc
- Neutralisation
by enzymes or
antibodes
- Death by
complement,
Ig and
lysosomes
- Opsonisation
by antibodies, collectins
and
complement (C3b)
- Phagocytosis and
Intracellular
destruction by
Macs
- Neutralisation
by enzymes or
antibodes
- Innate immunity
- Enzymes, Iron binding proteins (transferin
and lactoferin), defensins, interferons and
the complement cascade...
- Enzymes, Iron binding proteins (transferin
and lactoferin), defensins, interferons and
the complement cascade...
- Acquired Immunity
- Opsonization of encapsulated bacteria
allows phagocytosis- bind the Fc fragment
(string on soap) Opsonisation can occur via;
1) Collectins which recognise foreign C3b
and 2) Anti-bodies and C3b comps-
phagocytes have a receptor for C3b!
- Opsonization of encapsulated bacteria
allows phagocytosis- bind the Fc fragment
(string on soap) Opsonisation can occur via;
1) Collectins which recognise foreign C3b
and 2) Anti-bodies and C3b comps-
phagocytes have a receptor for C3b!
- TH2 antibody productionis the main response but there are essentially
four methods... This icludes the CLOSTRIDIAL disease- Tetani, Boltulium,
Bacillus and ENTERObactericae- Yersninia, Klebsiella etc
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