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type 1 diabetes mellitus (T1DM) 726 type II antibody-mediated hypersensitivity
Nerve Nerve
Activation of
muscle
Acetylcholine
Acetylcholine
receptor
Epitope
IgG
T lymphocyte
IgG
IgG
Activation of
muscle inhibited
Interference by acetylcholine receptor (AChR) antibodies with chemical
transmission of a nerve impulse. AChR antibodies are IgG autoantibodies
that cause loss of function of AChRs that are critical to chemical transmission
of nerve impulses at neuromuscular junctions. This event represents
a type II mechanism of hypersensitivity according to the Coombs and
Gell classification. AChRs are heterogeneous; some show specificity for
antigenic determinants other than those that serve as acetylcholine or
α-bungarotoxin binding sites. As many as 85 to 95% of myasthenia gravis
patients may manifest AChR antibodies.
cytokine receptors become dimerized. They signal through
JAK–STAT (Janus kinase–signal transducer and activator
of transcription) pathways.
type 1 diabetes mellitus (T1DM)
Insulin-dependent diabetes mellitus in which injury to
pancreatic β islet cells leads to loss of insulin synthesis
associated with autoimmunity. Associated with insulitis and
antibodies against pancreatic β islet cell antigens.
type 2 diabetes mellitus (T2DM)
Noninsulin-dependent diabetes mellitus characterized
by normal insulin production but failure of host cells to
respond to it. Not attributable to autoimmunity.
type I interferons (IFN-, IFN-)
Cytokines synthesized by virus-infected cells that inhibit
replication of virus by infected cells and alert bystander
r s
C1, 4, 2, 3, 5b,
6, 7, 8, 9
C1qrs complex
Formation
of membrane
attack
complex
(M.A.C.)
Action of specific IgG antibody on surface epitopes of a T lymphocyte, leading to antibody–complement-mediated lysis of the cell.
uninfected cells to arm themselves against infection. A
cytokine family of proteins comprised of several of the
IFN-α variety that are structurally similar together with
a single IFN-β protein. All the type I interferons manifest
potent antiviral activity. Mononuclear phagocytes represent
the principal source of IFN-α, whereas IFN-β is synthesized
by numerous cell types that include fibroblasts. The
same cell surface receptor binds both IFN-α and IFN-β,
both of which have similar biologic effects. Type I interferons
block viral replication, potentiate the lytic activity of
natural killer (NK) cells, enhance major histocompatibility
complex (MHC) class I expression on virus-infected cells,
and induce the development of human Th1 cells.
type II antibody-mediated hypersensitivity
A type of hypersensitivity induced by antibodies and
which appears in three forms. The classic type of
hypersensitivity involves the interaction of antibody with
cell membrane antigens followed by complement lysis.
These antibodies are directed against antigens intrinsic
to specific target tissues. Antibody-coated cells also have
increased susceptibility to phagocytosis. Examples of
type II hypersensitivity include the antiglomerular basement
membrane antibody that develops in Goodpasture’s
syndrome and antibodies that develop against erythrocytes
in Rh incompatibility, leading to erythroblastosis fetalis or
autoimmune hemolytic anemia. A second variety of type
II hypersensitivity is antibody-dependent cell-mediated
cytotoxicity (ADCC). Natural killer (NK) cells that have
Fc receptors on their surfaces may bind to the Fc regions
of immunoglobulin G (IgG) molecules. They may react
with surface antigens on target cells to produce lysis of the
antibody-coated cells. Complement fixation is not required
and does not participate in this reaction. In addition to
NK cells, neutrophils, eosinophils, and macrophages may
participate in ADCC. A third form of type II hypersensitivity
involves antibodies against cell surface receptors
that interfere with function, as in the case of antibodies
against acetylcholine receptors in motor endplates of
skeletal muscle in myasthenia gravis. This interference