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Biomedical subjects

K L Banks

Publications and source records attributed to K L Banks.

54 records · Page 3Linked to original sources
PubMed1976

Alterations of the thymus and other lymphoid tissue in young horses with combined immunodeficiency.

Combined immunodeficiency (CID) is a significant disease in terms of prevalence in Arabian foals and is a useful animal for study of a similar condition in children. Thymuses from all CID foals examined were extremely hypoplastic. Light and electron microscopic examination of thymuses from CID foals, as well as a thymus from an aborted CID fetus, demonstrate that the basic thymic structure is intact, despite a number of dissimilar morphologic appearances. From these data, we inferred that the thymic hypoplasia was caused by a failure of committed lymphocytes from the bone marrow to populate the organ. The lack of uniform organized lymphocytes in the spleen and lymph nodes provides considerable support for the absence of lymphoid precursors or their inability to respond to differentiating influences.

Animals↗
PubMed1976

In vitro synthesis of immunoglobulin and anti-viral antibody in Aleutian disease viral infection of mink.

Lymphoid cells from Aleutian disease virus (ADV)-infected and noninfected mink were cultured in vitro and the synthesis of Ig M, IgG, and viral-specific antibody measured. Compared to noninfected mink, lymph node cells from mink with Aleutian disease (AD) contained a higher percentage of plasma cells and immunoglobulin-bearing lymphocytes, synthesized significantly more IgG, and produced detectable quantities of ADV-specific antibody. No significant difference in IgM synthesis was observed.

Aleutian Mink Disease↗
PubMed1975

Hypogammaglobulinemia predisposing to infection in foals.

Measurement of serum immunoglobulins in 46 foals less than 2 weeks old revealed 9 foals with hypogammaglobulinemia. The hypogammaglobulinemia was attributed to failure in transfer of immunoglobulins from dam to foal via colostrum. Three of the affected foals did not nurse at all, or only slightly, and 2 of these died of infections within a few days after birth, whereas the 3rd foal did not grow as well as normal foals. Six of the affected foals nursed in an apparently normal manner, and 5 of these had nonfatal respiratory infections between 2 and 5 weeks of age. Analysis of serum samples from surviving foals demonstrated that immunoglobulins were eventually produced. One other foal examined had hypogammaglobulinemia at 57 days of age, an age when the foal should have produced large amounts of immunoglobulin independent of passive transfer. This foal had simultaneous infections and hypogammaglobulinemia, but eventually produced normal amounts of immunoglobulin. Cellmediated immunity was normal at 3 months of age. This condition was designated transient hypogammaglobulinemia and was thought to be due to a temporary inability to make immunoglobulins.

Adenoviridae Infections↗
PubMed1975

Regulation by antibody of phytolectin induced lymphocyte proliferation. I. Evidence for two mechanisms of suppression.

Studies were conducted to determine the mechanisms of antibody suppression of phytohemagglutinin (PHA)- and concanavalin A (Con A)-induced lymphocyte proliferation. Initial experiments incubated lymphocytes with either PHA or Con A, and at various times the respective anti-phytolectin was added to the cultures. DNA synthesis was less than 20% of the total response if anti-PHA was added within 2 hr and if anti-Con A was added within 10 hr of addition of mitogens to the culture. At the concentrations used, anti-PHA reduced PHA binding to the lymphocytes, while anti-Con A did not reduce Con A binding to the cells. Antibody was non-toxic and specific for its respective mitogen. Additional experiments incubated lymphocytes with either PHA or Con A and then the cells were washed and placed in mitogen-free media. The addition of antibody to cultures which had been washed markedly suppressed proliferation. Using radiolabeled PHA and Con A in one group of experiments and fluorescent labeled anti-mitogen antibodies in others, it was determined that antibody did not remove Con A or PHA from the cell, but instead antibody slowed the release of mitogen from the lymphocyte. Anti-mitogen antibody remained attached to mitogen on the surface of lymphocytes for at least 24 hr. The experiments suggest that antibody can suppress the lymphocyte reaction by blocking the necessary phytolectinlymphocyte interaction and interrupting stimulation by cell-bound mitogen.

Animals↗
PubMed1975

Lymphocyte abnormalities in Aleutian disease virus infection of mink: decreased T lymphocyte responses and increased B lymphocyte levels in persistent viral infection.

Persistence of virus and a marked hypergammaglobulinemia are consistent features observed in mink with Aleutian disease virus infection. These events may result from altered lymphocyte function in infected mink. To test this possibility we determined the ability of lymphocytes from infected mink to respond to phytolectins (PHA and Con A), and a specific antigen (KLH) in a lymphocyte transformation test and quantitated the number of lymphocytes bearing surface immunoglobulin. Infected mink had a significantly lower response than normal mink to PHA and Con A (P less than 0.025), and the difference in the responses increased progressively with time post-infection. Infected mink immunized with KLH also had a decreased ability to respond to this antigen when compared to normal immunized mink (P less than 0.001). The number of lymphocytes bearing surface immunoglobulin was significantly elevated in three of 10 mink infected for 10 weeks, and in all of seven mink infected 32 weeks (P less than 0.001).

Aleutian Mink Disease↗
PubMed1975

Surface receptors on neutrophils and monocytes from immunodeficient and normal horses.

Surface receptors on peripheral blood neutrophils and monocytes from normal and immunodeficient horses have been studied. Sheep erythrocytes (SRBC) coated with IgG, IgM, and complement but not IgG(T), readily bound to normal equine monocytes and neutrophils. More than 4000 molecules of IgG were required to sensitize each SRBC for adherence to monocytes, and more than 12,000 molecules were required for adherence to neutrophils. Young horses with a severe combined immunodeficiency had an almost total absence of lymphocytes, but normal numbers of monocytes and neutrophils. The number of receptors for immunoglobulin, complement, and phytolectin on monocytes and neutrophils from immunodeficient animals were similar to those on the cells of normal horses. Although the precursor cells of lymphocytes of horses with combined immunodeficiency appear to be defective, no defect in the other cellular products of the bone marrow were apparent.

Age Factors↗
PubMed1973

Quantitation of immunoglobulin-bearing lymphocytes and lymphocyte response to mitogens in horses persistently infected by equine infectious anemia virus.

A defect in lymphocyte function could be responsible for persistent infection by the equine infectious anemia virus. The number of lymphocytes bearing surface immunoglobulin, as detected by immunofluorescence, and lymphocyte response to mitogens were the same in uninfected and equine infectious anemia-infected animals. A defect in T or B lymphocyte numbers or ability to respond to stimuli was not detected in this chronic virus disease.

Animals↗