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Biomedical subjects

K L Banks

Publications and source records attributed to K L Banks.

At least 37 records · Page 2Linked to original sources
PubMed1982

Antigenic stimulation of T lymphocytes in chronic nononcogenic retrovirus infection: equine infectious anemia.

Equine infectious anemia is a chronic disease of horses caused by a nononcogenic retrovirus. Studies were undertaken to determine the types of cells involved in the in vitro lymphoproliferative response to viral antigens and the dynamics of this reaction. It was observed that reactive lymphocytes were present at unpredictable times in the peripheral blood of infected horses. This reaction was shown to be specific for the interaction of equine infectious anemia virus and T lymphocytes. Enriched B-lymphocyte populations did not divide when exposed to equine infectious anemia virus. Macrophages were depleted from the reaction by two methods: adherence to Sephadex and a combination of binding to Sephadex and adherence to complement-coated erythrocytes. Both methods reduced the number of monocytes, but only the combination of Sephadex and complement-coated cells removed the accessory cells needed for lymphocyte proliferation. We conclude that during the chronic stages of equine infectious anemia the number of antigen-reactive T lymphocytes fluctuates within the peripheral blood and that these cells require a complement-binding cell for reaction. The relationship of these cells to the lymphoproliferative stages of this disease is discussed.

Animals↗
PubMed1982

Early course of infection in susceptible and resistant strains of mice, using [3H]uridine-labeled Trypanosoma brucei subsp. brucei.

A radioisotopic technique utilizing [3H]uridine was developed to determine the tissue distribution of intravenously inoculated Trypanosoma brucei spp. brucei in susceptible (Swiss-Webster) and resistant (deer) strains of mice. The reliability of the technique was tested by using unincorporated [3H]uridine and heat-killed (labeled) trypanosomes in parallel experiments. The inoculations with viable (labeled) organisms showed that during the initial 24 h T. brucei subsp. brucei was cleared from the bloodstream of deer mice to a significantly greater extent than in Swiss-Webster mice. In addition, significantly more radioactivity was found in the liver, spleen, and kidneys of the deer mice. Autoradiographs of trypanosomes in selected tissues supported the distribution observed with labeled organisms. All of the above experiments involved the highly virulent, monomorphic bloodstream form of T. brucei subsp. brucei. Similar experiments with less virulent tissue culture-adapted trypanosomes showed that these organisms were readily cleared from the bloodstream, even in highly susceptible Swiss-Webster mice. The results suggest that avoidance of phagocytosis may be an important virulence factor of T. brucei subsp. brucei and contributes to the variation observed in species and strain susceptible to trypanosomiasis.

Animals↗
PubMed1982

Lymphocyte subpopulations of the goat: isolation and identification.

Experiments were designed to identify and isolate goat monocytes and lymphocytes. Leukocytes were obtained from peripheral blood, thymus, spleen, and lymph nodes. Thymocytes lacked surface immunoglobulin (Ig) detectable by immunohistochemical techniques and receptors for complement or Ig. A majority of the thymocytes nd nylon-wool purified blood T lymphocytes bound peanut agglutinin (PNA). However, a distinct minority of the T lymphocytes lacked receptors for PNA. The PNA nonreactive lymphocytes represented a greater portion of the cells of the spleen and lymph nodes, suggesting that caprine T lymphocytes may be placed in PNA reactive and nonreactive subpopulations. Lymphocytes with complement and Ig receptors and surface Ig were detected in the blood, spleen, and lymph nodes. These cells met the criteria for caprine B lymphocytes. The lymphocytes were enriched by immunocytoadherence techniques followed by isopyknic centrifugation, and the portion of PNA reactive cells decreased as the number of B lymphocytes increased.

Animals↗
PubMed1981

An evaluation of contribution derived from investigations of equine immunodeficiencies.

Following the descriptions of immunodeficiencies in horses beginning in 1973, there has been considerable effort to develop methods for differential diagnosis and to determine the cause and prevalence of the disorders. In addition, the equine immunodeficiencies, especially combined immunodeficiency, have been studied from a comparative viewpoint with the goal of finding information applicable to similar diseases of children. Coincident with the development of knowledge about the immunodeficiencies per se, considerable information about several aspects of immunology has been obtained. It is the purpose of this review to focus on findings from experiments with equine immunodeficiencies concerning prenatal and neonatal immunology, lymphocyte function, secretory immunity, immunoreconstitution, graft-versus-host reactions and previously unrecognized diseases.

Animals↗
PubMed1981

Isolation and identification of equine lymphocytes and monocytes.

Various cell populations of equine mononuclear leukocytes were identified and isolated. Mononuclear leukocytes were concentrated by isopyknic centrifugation, using a solution of Ficoll and Hypaque. Three additional techniques were explored to separate monocytes from lymphocytes, and 3 methods were used to separate lymphocyte types. Cytochemical techniques for the detection of nonspecific esterase readily distinguished equine monocytes from lymphocytes. Peripheral blood lymphocytes were separated into at least 2 populations. One population had surface traits identical to thymocytes [ie, they readily bound peanut agglutinin, but lacked receptors for complement or immunoglobulin (Ig) and did not have surface Ig, as detected by immunohistochemical techniques]. This population could be isolated, using nylon-wool columns, or by depletion of complement- and Ig-binding cells during centrifugation. The other class of lymphocytes had equine complement receptors, Ig receptors, and detectable surface Ig, but was not bound by peanut agglutinin. Using rosetting techniques followed by centrifugation, this latter population was enriched. These studies provided means of isolating and detecting equine monocytes, B lymphocytes, and T lymphocytes.

Animals↗
PubMed1981

Collection and cultivation in vitro of equine mammary macrophages.

Equine macrophages were obtained from female Shetland ponies by injection of Escherichia coli lipopolysaccharide through the lactiferous ducts of the mammary gland. After 6 to 11 days, balanced salt solution was injected into the mammary gland to wash out accumulated cells. Harvested cells contained a mixture of macrophages, lymphocytes, and neutrophils, with the majority of the cells of mononuclear type. In culture, cells adherent after 24 hours were characterized as macrophages by morphologic features, nonspecific esterase staining, and by the presence of complement and immunoglobulin receptors. These cultures were grown to a variety of culture media. A basal medium, consisting of 15% equine serum and 10% bovine fetal serum in conjunction with RPMI 1640 medium containing 20 mM HEPES buffer, was the most effective for maintaining spreading and adhesion of cells. Conditioned medium from mouse fibroblast cultures (L cells), added at 30% to the basal medium, improved cell monolayers by reducing giant cell formation and prolonging cell adhesion.

Animals↗
PubMed1980

Immune responses of goats persistently infected with caprine arthritis-encephalitis virus.

Eight cesarean-derived goat kids were inoculated with caprine arthritis-encephalitis virus (CAEV), and proliferative responses of their peripheral blood mononuclear cells to mitogens and CAEV antigen were monitored for 9 months. Antibody specific for CAEV was measured by an enzyme-linked immunosorbent assay. Five cesarean-derived noninfected goats were tested simultaneously. Significant differences between the infected and control mononuclear cell proliferation reactions to CAEV began 14 days post-inoculation and continued in a fluctuant manner until 134 days post-inoculation. The magnitude of the proliferative reaction steadily increased in infected goats until the end of the experiment at 271 days post-inoculation. Responses to mitogens were not significantly different between infected and control goats. Virus-inoculated goats produced CAEV-specific antibody that reached a maximum level between 49 and 77 days post-inoculation and then declined to lower levels through 271 days post-inoculation. The virus-inoculated goats developed mild but characteristic clinical evidence of caprine arthritis-encephalitis, and CAEV was reisolated from four goats at 286 days post-inoculation. The five control goats developed neither an anti-CAEV immune response nor clinical disease, and CAEV could not be reisolated from them.

Animals↗
PubMed1980

Injury induced by Trypanosoma congolense adhesion to cell membranes.

Trypanosoma congolense binds to erythrocytes and the walls of the microvasculature. Experiments were conducted to determine if the attachment of T. congolense, alone or in combination with antitrypanosome antibody, was damaging to host cells. Bovine erythrocytes were labelled with 51Cr and incubated with T. congolense to promote adhesion. Plasma from the same donor as the red blood cells was added to the erythrocyte-trypanosome aggregates and the release of 51Cr measured. There was a two- to threefold increase in 51Cr release when trypanosomes were lysed by antibody-complement interaction following adhesion to the erythrocyte. The erythrocytes were not damaged by trypanosome binding in the absence of antibody or complement. A similar mechanism may operate in vivo because experiments demonstrated an increased vascular permeability of mesenteric vessels, a site of T. congolense attachment to the microcirculation. These results suggest that the adhesion of T. congolense to host cells, followed by an immune response to the parasite, may damage the infected host by "innocent bystander" mechanisms.

Animals↗
PubMed1979

In vitro binding of Trypanosoma congolense to erythrocytes.

Trypanosoma congolense Broden, an intravascular parasite, binds to vessel walls and erythrocytes of infected hosts. In an attempt to characterize T. congolense adhesion to host cells, an in vitro assay was devised. It was shown in the in vitro experiments that T. congolense binds to bovine, sheep, and goat erythrocytes, but not always to erythrocytes of rats, mice, rabbits, horses or humans. Only the anterior part of live trypanosomes adheres to erythrocytes, and the attachment site on the trypanosomes is destroyed by trypsin and chymotrypsin-trypanosomes did not adhere to bovine erythrocytes that had been incubated with neuraminidase, sodium periodate and poly-L-lysine. The foregoing experiments suggest that the surface of T. congolense contains a protein-associated site which binds to sialic acid of some host cells. This surface site is most likely responsible for attachment to blood vessels in vivo.

Animals↗
PubMed1978

Binding of Trypanosoma congolense to the walls of small blood vessels.

The mesenteric microvasculature was studied in rats and rabbits infected with Trypanosoma congolense. By examining vessels in the living animals, trypanosomes were observed to adhere to vessel walls by their anterior ends. It was evident from stained preparations of the vessels that the microcirculation contained 4-1400 times as many trypanosomes as were free in the cardiac blood. Parasites were more numerous in very small vessels than in larger vessels, and they were clustered in groups within the small vessels. The localization of T. congolense in the microvasculature is demonstrated and it is shown that this localization is established by attachment of the organism to the vessel wall.

Animals↗
PubMed1978

In vitro and in vivo effects of corticosteroids on peripheral blood lymphocytes from ponies.

The in vitro and in vivo effects of corticosteroids on peripheral blood lymphocytes (PBL) from ponies were studied. Prednisolone inhibited lymphocyte stimulation by phytohemagglutin (PHA) in a dose-dependent manner, without inducing lysis even at large doses. The PBL from horses heterozygous for the combined immunodeficiency trait responded to corticosteroid treatment the same as did PBL from normal ponies. Removal of the corticosteroid after incubation with PBL from normal ponies partially restored responsiveness of these cells to PHA. Chronic in vivo treatment of ponies with corticosteroids caused a marked decrease in the absolute numbers of circulating lymphocytes. Most remaining lymphocytes had detectable surface immunoglobulin and C3 receptors, suggesting a greater decrease in the T-lymphocyte population. In spite of this, there was little change in the in vitro PHA- or keyhole limpet hemocyanin-sensitized ponies. In general, the corticosteroid effects of lysis, as well as the mitogenic and antigenic responses of PBL from ponies, were similar to those previously reported for human lymphocytes.

Animals↗
PubMed1978

Regulation by antibody of lectin-induced lymphocyte proliferation: antibody inhibition of mitogenesis and release of lectin from cell surfaces.

Studies were conducted to determine the ways in which antibody regulates proliferation of lymphocytes stimulated by phytohemagglutinin (PHA) and concanavalin A (ConA). Equine lymphocytes were reacted with PHA or ConA for 1 to 10 hours, washed free of excess lectin, then cultured for 3 days and examined for proliferation and incorporation of [3H]thymidine. Both PHA and ConA induced lymphocytes to proliferate after short incubation periods. This response could be interrupted by the addition of antibody to the respective lectin. Total suppression of the proliferative response occurred if antibody was added within the first 2 hours after initial contact with PHA or ConA. Addition at times up to 48 hours produced either total or partial suppression. The removal of excess antibody 4 hours after addition to the culture did not reverse the suppression. Using radiolabeled ConA and PHA, it was observed that suppressive antibody inhibited the release of lectin from metabolically active lymphocytes and from surfaces where pinocytosis was not possible or was minimized. Antibody did not affect the rate of degradation of lectin by the cells. These results indicate that antibody attached to lectins, already bound to the lymphocyte surface, can terminate the lymphocyte response and retard the rate of release of lectin from the cell membrane.

Antibodies↗
PubMed1976

Agammaglobulinemia in a horse with evidence of functional T lymphocytes.

Agammaglobulinemia was diagnosed in a 1-year-old Thoroughbred horse on the basis of the following observations: (1) absence of serum immunoglobulins M, A, and G(T); (2) small amounts of serum immunoglobulin G (16 mg/100 ml); (3) absence of specific antibody in the serum of the horse following immunization and challenge exposure to 2 antigens; (4) absence of plasma cells, primary follicles, and germinal centers in a lymph node removed after antigenic stimulation; (5) absence of "natural" serum antibodies to rabbit-erythrocytes which were easily detectable in age-matched control horse serums; and (6) increased susceptibility to infections. There was evidence of functional cell-mediated immunity which included a skin response to injected phytolectins, skin response to antigen challenge following sensitization, and in vitro proliferative response of lymph node cells to phytohemagglutinin. An intact cell-mediated immune response was also supported by the observation that the horse lived to 17 months of age without antibody production, whereas horses with an absence of both antibody production and cell-mediated immunity (combined immunodeficiency) die by 4 months of age without immunologic intervention. The known features of agammaglobulinemia in this horse are similar to those in sex-linked agammaglobulinemia in persons and are unique among the immunodeficiences described in other animals.

Agammaglobulinemia↗