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Toxicolgy
Immunology
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Created by
Ella Briggs
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Cards (25)
In the bone marrow, immune cells begin as
myeloid
and
lymphoid
progenitors
Dendrites
act as
antigen
presenting cells
Toll-like receptors
recognise
PAMPS
Cellular
stress can be seen in the form of
DAMPS
Antigen presenting cells
will contain peptides and
MHC
inside
MHC
on surface along with the release of cytokines causes the maturation of a naive
T cell
into a
T helper cell
The
combination
of signals needed is what protects us against
overactivation
Antigens
can form a
covalent
bond with large peptide compounds. This leads to the formation of a
hapten
-
carrier
conjugate
Haptens
are too small to elicit an immune reaction on their own
The formation of a
hapten-conjugate complex
produces a
complete antigen
which is large enough to trigger and immune response
APCs
also contain
co-stimulatory
molecules on their surface
Adjuvants
can upregulate
costimulation
TH2 cells
leads to
memory B cell
formation
TH1 cells
leads to
memory T cell
formation
Type 1 hypersensitivity occurs immediately
Allergens
binding to
IGE
causes
crosslinking
causes
degranulation
of mast cells and release of
mediators
(
Hypersensitivity
1)
Key symptoms of
hypersensitivity
1
are skin reactions and itching
Type IV hypersensitivity
causes a delayed reaction
Type IV
is associated with the production of
memory T cells
A
hapten
forms a protein conjugate at the
epidermis
and is processed by
langerhan
cells (Type IV)
Dendrite
presents
hapten
to
memory T cells
Release of
cytokines
Migration of
inflammatory cells
Type IV hypersensitivity
can take up to
48
hours for a reaction to occur.
Lipid soluble molecules
can interact with
intracellular peptides
. This leads to presentation of antigen and
MHC
on surface causing tissue damage
Allergies
can develop due to co-exposure to other pollutants
Neutrophils
have a
half life
of
3
days meaning encountering a second compound can leads to reduced immune function
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