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myc 517 mycophenolate mofetil
and animals immunized against AChR develop circulating
antibodies and clinical manifestations of MG. A subgroup
of patients have seronegative MG; they resemble classic MG
patients clinically but have no anti-AChR antibodies in their
circulation. Because the IgG anti-AChR autoantibodies cross
the placenta from mother to fetus, newborns of mothers with
this disease may also manifest signs and symptoms. Neonatal
MG establishes the antibody-mediated autoimmune nature
of the disease. The thymus of an MG patient may reveal
lymphofollicular hyperplasia (70%) or thymoma (10%). Anti-
AChR-synthesizing B cells and T helper lymphocytes may
be found in hyperplastic follicles. These are often encircled
by myoid cells that express AChR. Interdigitating follicular
dendritic cells closely associated with myoid cells have been
suggested to present AChR autoantigen to autoreactive T
helper lymphocytes. Anti-idiotypic antibodies have been used
to suppress or enhance experimental autoimmune myasthenia
gravis (EAMG), depending on the antibody concentration
employed. Conjugate immunotoxins to anti-Id antibodies
have been able to suppress autoimmunity to AChR. Both
thymectomy and anticholinesterase drugs have proven useful
in treatment.
myc
An oncogene designated v-myc when isolated from an avian
myelocytomatosis retrovirus and c-myc when referring
to the cellular homolog. Two others designated N-L-myc
have been cloned. myc Genes are activated by overexpression
by upregulation caused by transcriptional regulatory
signal mutations in the first intron or by gene amplification.
Normal tissues contain c-myc. When c-myc is in its normal
position on chromosome 8, it remains transcriptionally
silent, but when it is translocated, as in Burkitt’s lymphoma,
it may become activated. The protooncogene c-myc is
amplified in early carcinoma of the uterine cervix and lung
and in promyelocytic leukemia.
mycobacteria immunity
Immunity to tuberculosis is highly complex and involves
cell-mediated mechanisms. The host immune response
to tuberculosis is inappropriate, leading to tissue injury
through immune mechanisms rather than elimination of the
invading microorganism. In mice, immunity depends upon
TNF-α, a Th1 cytokine pattern, and MHC class II. Mouse
murine macrophages activated by IFN-γ inhibit proliferation
of M. tuberculosis. β 2 microglobulin is requisite for immunity
to mycobacteria which may point to the participation
of CD8 + MHC class I restrictor cytotoxic T cells. γδ T cell
receptors identify mycobacterial antigens such as heat-shock
proteins. These cell types secrete IFN-γ and are cytotoxic
and classified as a type I response. A type II response
renders mice more susceptible to tuberculosis. Immunity in
humans is also associated with a Th1 type of response associated
with macrophage activation and cytotoxic removal
of infected cells. Human tuberculosis patients form specific
IgE and IgG 4 antibodies, both of which are IL4-dependent.
IL10 levels may also be increased. A Th2 response is associated
with progressive disease in humans. M. tuberculosis
can cause release of TNF-α from primed macrophages.
This cytokine is requisite for protection but also has a role
in immunopathology. Patients with tuberculosis develop
necrotic lesions believed to help wall off established infections.
The TNF-α toxicity in a mycobacterial lesion depends
on whether the T cell response is Th1 or Th2. Necrosis is not
produced when TNF-α is injected into a Th1 inflammatory
site, but marked tissue injury results when it is injected into
a Th1/Th2-mediated site. Infection by M. leprae is weakly
associated with MHC haplotypes. It appears to determine
the type of disease that will develop instead of susceptibility.
In tuberculoid leprosy, both in vivo and in vitro equivalents
of T cell-mediated responsiveness such as skin test reactivity
in lymphoproliferation in response to antigens of M. leprae
are intact. Th1 cytokines are produced in these lesions.
Unless treated, they will develop into lepromatous leprosy
in which the Th1 response is impaired. In leprosy, immunity
probably requires macrophage activation and cytotoxic T
cells activated by the Th1 response. In lepromatous leprosy,
T cell-mediated immunity is depressed in vivo and in vitro.
Numerous macrophages packed with bacilli are present in
the lesions, but no response occurs. There is a continuous
heavy antigen load and lack of a T cell-mediated response
to the microorganism. The T cells express a Th2 cytokine
pattern.
mycobacterial adjuvants
Substances used to enhance both humoral and cellular
immune responses to antigen. Killed, dried mycobacteria,
including Mycobacterium tuberculosis among other
strains, are ground and suspended in lightweight mineral
oil. With the aid of an emulsifying agent such as arlacel
A, added antigen in aqueous medium is incorporated to
produce a water-in-oil emulsion used for immunization.
The mycobacteria are especially effective in stimulating
cell-mediated immunity to the antigen. The administration
of this adjuvant without antigen may induce adjuvant
arthritis in rats. Incorporation of normal tissues such as
thyroid or adrenal into Freund’s complete adjuvant may
induce autoimmune disease if reinoculated into the animal
of origin or other members of the strain with the same
genetic background.
mycobacterial peptidoglycolipid
A constituent of the wax D fraction of Mycobacterium
tuberculosis var. hominis that contains the component
associated with such mycobacterial adjuvants as Freund’s
adjuvant. Under electron microscopy, the peptidoglycolipid
exhibits a homogeneous, intertwined filamentous structure.
Mycobacterium
A genus of aerobic bacteria including Mycobacterium
tuberculosis that can survive within phagocytic cells and
produce disease. Cell-mediated immunity is the principal
host defense mechanism against mycobacteria.
O
O
OH
CH 3
OCH 3
CH3
mycophenolate mofetil
A semisynthetic derivative of mycophenolic acid isolated
from the mold Penicillum glaucum. An immunosuppressive
agent used to prolong survival of allogeneic transplants
including kidney, heart, liver, intestine, limb, small bowel,
O
O
Structure of mycophenolate mofetil.
N
•HCl
O
M