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heavy chain subclass 314 Helicobacter pylori immunity
in which patients produce excess incomplete α chains of
IgA 1 molecules. It mainly affects Sephardic Jews, Arabs,
and other Mediterranean residents, as well as subjects in
South America and Asia. It may appear in childhood or
adolescence as a lymphoproliferative disorder associated
with the respiratory tract or gastrointestinal tract. Patients
may manifest malabsorption, diarrhea, steatorrhea, hepatic
dysfunction, weight loss, lymphadenopathy, hypocalcemia,
and extensive mononuclear infiltration. α Heavy chain
disease may either spontaneously remit or respond favorably
to treatment with antibiotics; it may require chemotherapy
in some cases. δ Heavy chain disease has been
reported in an elderly male demonstrating abnormal plasma
cell infiltration of the bone marrow along with osteolytic
lesions. γ Heavy chain disease (Franklin’s disease) occurs
in older men, and may induce death rapidly (within weeks)
or last for years. Death usually takes place within 1 year
because of infection. Patients develop lymphoproliferation
with fever, anemia, fatigue, angioimmunoblastic lymphadenopathy,
hepatosplenomegaly, eosinophilic infiltrates,
leukopenia, lymphoma, autoimmune disease, or tuberculosis.
Serum IgG 1 is elevated. γ Heavy chain disease has been
treated with cyclophosphamide, vincristine, and prednisone.
μ Heavy chain disease is a rare condition affecting middleaged
to older individuals. Some patients may ultimately
develop chronic lymphocytic leukemia. μ Heavy chain disease
is characterized by lymphadenopathy, hepatosplenomegaly,
infiltration of the bone marrow by vacuolated plasma
cells, and frequently elevated synthesis of κ light chain.
heavy chain subclass
Within an immunoglobulin heavy chain class, differences
in primary structure associated with the constant region
that can further distinguish these heavy chains of the same
class are designated as subclasses. These differences are
based on primary or antigenic structure. The heavy chain
subclasses are designated γ 1, γ 2, γ 3, etc.
Michael Heidelberger.
Heidelberger, Michael (1888–1991)
An American considered the father of immunochemistry.
He began his career as an organic chemist. His contributions
to immunology include the perfection of quantitative
Michael Heidelberger, who purified the first component of complement
and showed that complement was real, had weight, and contained protein.
immunochemical methods and the immunochemical characterization
of pneumococcal polysaccharides. His contributions
to immunologic research are legion. He received the
Lasker Award, the National Medal of Science, the Behring
Award, the Pasteur Medal, and the French Legion of Honor.
(Refer to Lectures on Immunochemistry, 1956.)
Helicobacter pylori immunity
Both circulating and local humoral antibody responses follow
H. pylori colonization of the gastric mucosa. During the
prolonged mucosal infection, IgG 1 and IgG 4 and often IgG 2
antibodies are detectable but IgG 3 and IgM antibodies only
rarely. IgA antibodies are usually also present. The initial
IgM response is followed later by IgA with conversion to
IgG 22 to 33 days after infection. IgA antibodies are found
at the local mucosal level and are secreted into the gastric
juice. IgG produced locally is rapidly inactivated when it
reaches the gastric juice. A systemic IgG response is present
throughout the infection and diminishes, only prolonging
successful therapy. If the infection reappears, the IgG antibody
titer rises. The specificity of circulating host antibody
against H. pylori varies greatly. This is attributable in part to
variations in host response and to a lesser degree to antigenic
diversity of the microorganisms such as variation in the Vac
A and Cag A proteins. Most infected subjects synthesize
antibodies against numerous antigens, including the urease
subunits, the flagellins, and the 54-kDa HSP60 homolog.
Antibodies usually develop to Vac A and Cag A polypeptides
if they are present in the infecting strain. Although of
variable complexity, the antigens all include urease. Plasma
cells, lymphocytes, and monocytes infiltrate the superficial
layers of the lamina propria in H. pylori-associated gastritis.
Half of the mature B cells and infiltrate are B cells producing
mostly IgA but also IgG and IgM. These cells produce
antibodies specific for H. pylori and are mostly of the CD8 +
subset, although CD4 + T cells are also increased, as well
as γδ T cells. Gastric epithelial cells aberrantly express
HLA-DR during H. pylori infection, which is also associated
with elevated synthesis of IL1, IL6, and TNF-α in the gastric
mucosa. H. pylori induces IL1, IL6, and TNF-α in the gastric
mucosa. It also induces IL8 expression in gastric epithelium
which induces neutrophil chemotaxis; 92% of non-Hodgkin
lymphoma cases affecting the stomach are associated with
H. pylori infection. The bacteria may engage in immune
avoidance by continually losing highly antigenic materials
such as urease and flagella sheaths from the bacterial surface,