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Mycoplasma–AIDS link 518 myelin autoantibodies
pancreatic islets, and bone marrow. This immunosuppressive
drug induces reversible antiproliferative effects specifically
on lymphocytes but does not induce renal, hepatic,
and neurologic toxicity. Its action is based on the requirement
for adequate amounts of guanosine and deoxyguanosine
nucleotides for lymphocytes to proliferate following
antigenic stimulation. Thus, an agent that reversibly inhibits
the final steps in purine synthesis, leading to a depletion
of guanosine and deoxyguanosine nucleotides, may induce
effective immunosuppression. Mycophenolate mofetil was
found to produce these effects. It is the morpholinoethyl
ester of mycophenolic acid. In vivo, it is hydrolyzed to the
active form, mycophenolic acid glucuronide, which is biologically
inactive and excreted in the urine. Mycophenolate
blocks proliferation of peripheral blood mononuclear cells
of humans to both B and T cell mitogens. It also blocks
antibody formation as evidenced by inhibition of a recall
response by human cells challenged with tetanus toxoid.
Its ability to block glycosylation of adhesion molecules that
facilitate leukocyte attachment to endothelial cells and target
cells probably diminishes recruitment of lymphocytes
and monocytes to sites of rejection or chronic inflammation.
It does not affect neutrophil chemotaxis, microbicidal
activity, or superoxide production. In vivo, mycophenolate
prevents cytotoxic T cell generation and rejection of allogeneic
cells. It inhibits antibody formation in a dose-dependent
manner and effectively prevents allograft rejection
in animal models, especially when used in conjunction
with cyclosporine. Mycophenolate mofetil is effective in
the treatment of refractory rejection in solid organ transplant
recipients and in combination with prednisone as an
alternative to cyclosporine or tacrolimus. It is also used
for therapy of steroid-refractory graft-vs.-host disease
in hematopoietic stem cell transplant patients. It is used
with tacrolimus to prevent graft-vs.-host disease, and has
been suggested for use in autoimmune disorders including
lupus nephritis and rheumatoid arthritis. Toxicities include
gastrointestinal disturbances, headache, hypertension, and
reversible myelosuppression (principally neutropenia). It is
used to reverse acute rejection in canine renal and rat cardiac
allograft models. It inhibited proliferative arteriopathy
in experimental models of aortic and heart allografts in rats
and in primate cardiac xenografts. It inhibits immunologically
mediated inflammatory responses in animal models
and inhibits tumor development and prolongs survival in
murine tumor transplant models. It is absorbed rapidly
following oral administration and hydrolyzed to form mycophenolic
acid, the active metabolite. Mycophenolic acid is
a potent, selective, uncompetitive, and reversible inhibitor
of inosine monophosphate dehydrogenase and, therefore,
inhibits the de novo pathway of guanosine nucleotide
synthesis without incorporation into DNA. Since T and B
cells depend for their proliferation on de novo synthesis of
purines unlike other cell types that can utilize salvage pathways,
mycophenolic acid has potent cytostatic effects on
lymphocytes. It inhibits proliferative responses of T and B
lymphocytes to both mitogenic and allospecific stimulation.
It also suppresses antibody formation by B cells and inhibits
the glycosylation of lymphocyte and monocyte glycoproteins
involved in intercellular adhesion to endothelial cells;
it may inhibit leucocyte recruitment to sites of inflammation
and graft rejection.
Mycoplasma–AIDS link
A mechanism postulated by Luc Montagnier for AIDS
development. HIV-1 virus binds to cells first activated by
Mycoplasma infection.
mycoplasma immunity
High-titer cold agglutinin autoantibodies against sialooligosaccharide
of the Ii antigen type are sometimes found
during Mycoplasma pneumoniae infections. The first line
of defense against these microorganisms is phagocytosis,
yet mycoplasmas can survive neutrophil phagocytosis if
specific antibodies are not present. Secretory IgA is significant
in preventing localized colonization, but systemic
antibodies protect from primary infection and secondary
spread from localized colonization. Mycoplasmas can evade
the humoral immune response by undergoing antigenic
variation of surface antigens. T cells also appear to play
a role in immunity to mycoplasma that should be further
investigated.
mycoses
Diseases produced by fungus infection.
mycosis fungoides
A chronic disorder involving the lymphoreticular system.
The skin appears scaly and exhibits eczematous areas that
are erythematous, with infiltration by lichenified plaques.
Finally, ulcers and neoplasms of the internal organs and
lymph nodes develop. Cells in skin lesions reveal markers
that identify them as T lymphocytes. This disease usually
appears after 50 years of age and is more frequent in males
than females and in blacks than Caucasians. The number of
null cells in the blood circulation increases, with a simultaneous
decrease in the numbers of B and T lymphocytes. T cell
immunity is diminished both in vitro and in vivo, as revealed
by diminished lymphocyte unresponsiveness to mitogens
and by a poor response and skin test. Immunoglobulin A and
E levels may be elevated in the serum. A type of cutaneous T
cell non-Hodgkin lymphoma.
myelin-associated glycoprotein (MAG) autoantibodies
Autoantibodies against the glycoprotein constituent of myelin
that are found in the periaxonal region, Schmidt– Lanterman
incisures, lateral loops, and outer mesaxon of the myelin
sheath; belong to the immunoglobulin superfamily; and act as
adhesion molecules that facilitate myelination. MAG autoantibodies
recognize the N-linked L1 and J1 carbohydrate moiety,
which is also found on PO and P2 glycoproteins, sulfate-3glucuronyl
paragloboside (SGPG), and sulfate-3-glucuronyl
lactosaminyl paragloboside (SGLPG) glycolipids of peripheral
nerves, neural cell adhesion molecules, and Li and J1 of lymphocytes
and human natural killer cells. MAG autoantibodies
are present in half of polyneuropathy patients with monoclonal
gammopathy, which may be associated with other lymphoid
proliferative diseases. T lymphocyte responses to MAG have
been found in multiple sclerosis.
myelin autoantibodies
The detection of autoantibodies to myelin used previously to
screen for autoantibodies in idiopathic and paraproteinemic
neuropathy patients leads to inconsistent results due to imprecise
myelin preparations leading to poor clinical specificity.
Autoantibodies against myelin in Guillain–Barré syndrome
(GBS) and sensory polyneuropathy with monoclonal gammopathy
of unknown significance involve autoantibodies
against glycolipids, including sulfatide, Forssman antigen,
galactosyl–cerebroside (Gal–Cer) and gangliosides.