Untitled - D Ank Unlimited

wire loop lesion 751 Wright, Almroth Edward (1861–1947)
Tumor
target
cells
Tumor
growth
inhibited
+
Tumor
growth
continues
Winn assay.
Effector
lymphocytes
mice. Growth of the transplanted cells follows. T lymphocytes
that are specifically immune to the tumor cells will
inhibit tumor growth and provide information related to
tumor immunity.
wire loop lesion
Thickening of capillary walls as a result of subendothelial
immune complex deposits situated between the capillary
endothelium and the glomerular basement membrane. Wire
loop lesions are seen in diffuse proliferative lupus nephritis
and are characteristic of class IV lupus erythematosus.
They may also be seen in progressive systemic sclerosis and
appear with crescent formation, necrosis, and scarring.
Wiskott–Aldrich syndrome
blood lymphocytes
(note scarcity of surface
microvilli)
Normal blood lymphocyte
Wiskott–Aldrich syndrome.
Wiskott–Aldrich syndrome
X-linked recessive immunodeficiency disease of infants
characterized by thrombocytopenia, eczema, and increased
immunoglobulin A (IgA) and IgE levels. It is a consequence
of mutations in the WAS protein (WASP) that may have a
role in the survival and/or function of hematopoietic stem
cells, platelets, and lymphocytes. This protein connects
several membrane receptors to the cytoskeleton. A defect
in this protein could cause abnormal cellular morphology
or defective lymphocyte activation signals. Cell-mediated
immunity and delayed hypersensitivity are decreased, and
the antibody response to polysaccharide antigens is defective,
with only minute quantities of IgM appearing in the
serum. The condition may involve inability to recognize
processed antigen. It is a genetic disease characterized by
defective interactions of T cells and B cells. Male patients
may have small platelets with no surface glycoprotein Ib.
There is increased susceptibility to infection by pyogenic
bacteria. IgA and IgE are increased and IgM is diminished,
although IgG serum concentrations are usually normal.
Under electron microscopy, T lymphocytes appear bereft of
markedly fimbriated surfaces of normal T cells.
T lymphocytes have abnormal sialophorin. Patients may
have increased incidence of malignant lymphomas. Bone
marrow transplantation corrects the deficiency.
Noel Rose (left) and Ernest Witebsky (right), members of the Buffalo
Immunology Group.
Witebsky, Ernest (1901–1969)
German-American immunologist and bacteriologist who
made significant contributions to transfusion medicine
and concepts of autoimmune diseases. He was a direct
descendant of the Ehrlich school of immunology, having
worked at Heidelberg with Hans Sachs, Ehrlich’s principal
assistant, in 1929. He went to Mt. Sinai Hospital in New
York in 1934 and became a professor at the University
of Buffalo in 1936, where he remained until his death. A
major portion of his work on autoimmunity was the demonstration
with Noel R. Rose of experimental autoimmune
thyroiditis.
Witebsky’s criteria
According to criteria suggested by Ernest Witebsky, an
autoimmune response should be considered as a cause
of a human disease if (l) it is regularly associated with
that disease, (2) immunization of an experimental animal
with the antigen from the appropriate tissue causes an
immune response (formation of antibodies or development
of allergy), (3) the animal develops pathological changes
associated with this response that are basically similar to
those of humans, and (4) the experimental disease can be
transferred to a nonimmunized animal by serum or lymphoid
cells.
worms
Four types of cells are present in the earthworm coelom, all
of which are phagocytic. Some cells participate in allograft
rejection, whereas others synthesize antibacterial substances.
Wright, Almroth Edward (1861–1947)
British pathologist and immunologist who graduated as a
doctor of medicine from Trinity College, Dublin in 1889.
He became a professor of pathology at the Army Medical
School in Netley in 1892 and became associated with
the Institute of Pathology at St. Mary’s Hospital Medical
School, London, in 1902. He and Douglas formulated a
theory of opsonins and perfected an antitoxoid inoculation
W