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E Rabellino

Publications and source records attributed to E Rabellino.

10 recordsLinked to original sources

The level of differentiation of megakaryocyte progenitors and the subsequent modulation of megakaryocyte antigens on developing colony cells.

Human megakaryocyte development was studied in cell culture by first determining the differentiation stage of the clonable progenitor cell population and then analyzing the kinetics of expression of two megakaryocyte antigens using an immunoalkaline phosphatase system. Studies on the expression of two antigens present on megakaryocytes but not detectable on platelets (Mk-A, Mk-B) revealed that Mk-A antigen was found on megakaryocytes in colonies of less than six to eight cells at early times of cell culture. By contrast, Mk-B antigen was detected only in large megakaryocytes starting day 7 of culture and observed primarily in colonies of greater than eight cells. These studies show that human megakaryocyte progenitors are among the more mature of the precursor classes and link the antigen A bearing megakaryocytes to the developmental sequence as the immediate progeny of the precursor population with limited mitotic capacity. Amplification of antigen B expression is late in the developmental process, being detected by this method on only large megakaryocytes in well-formed colonies after 7-9 days of culture.

Agar

Aging and arteriosclerosis. Cell cycle kinetics of young and old arterial smooth muscle cells.

Intimal cell proliferation is a "hallmark" of atherosclerosis. Myointimal hyperplasia in arteries has been shown to be dependent on age after vascular endothelial denudation and injury associated with vascular transplantation. Because myointimal thickening is greater in aged rats than in younger rats, and aortic segments from old rats transplanted into young syngeneic recipients have a greater myointimal proliferative response to injury than its host environment, the authors examined the cell cycle distributions of old and young rat arterial smooth muscle cells (SMCs) by flow-cytometric analysis. They observed that there is an apparent age-dependent variation in the cell cycle distribution. Moreover, old SMCs have a greater percentage of their population in the S phase and not G2/M, compared with young SMCs; and there is a decrease in the percentage of old cells in the G0/G1 phase as compared with young SMCs. These differences may reflect the cellular changes observed during myointimal hyperplasia following vascular injury. It is concluded that our data support the hypothesis that the proliferation of SMCs is dependent, in part, on those processes related to aging as well as to the phenotypic state of the cell.

Aging

Immunoglobulins on the surface of lymphocytes. II. The bone marrow as the main source of lymphocytes with detectable surface-bound immunoglobulin.

Immunofluorescent studies using live cells from antibody-forming organs and anti-immunoglobulin antibodies demonstrate two populations of small lymphocytes which are differentiated by the presence or absence of Ig on their surface membranes. Most of the lymphocytes with detectable surface Ig appear to derive from cells of the bone marrow, while most of the Ig-negative lymphocytes derive from the thymus. Thus, adult mice thymectomized, lethally irradiated, and transplanted with bone marrow cells showed a normal number of lymphocytes with surface Ig but were depleted of the Ig-negative lymphocytes. Injection of thymocytes into these mice did not result in an increase in the number of lymphocytes with surface Ig in spleen and lymph nodes. Most of the injected thymocytes could be identified by means of histocompatibility markers. Also, the spleen and lymph nodes of neonatally thymectomized mice contained lymphocytes with surface Ig but were depleted of the Ig-negative lymphocytes. Attempts were made to identify light chains on thymocytes by a sensitive radioimmunoassay. In some experiments no light chains were detected and in others a small amount, i.e. no more than 2.6% of the amount present on spleen lymphocytes, could be detected. Whether these low figures are significant or represent a small amount of serum contamination is not clear as yet.

Animals

Immunoglobulins on the surface of lymphocytes. I. Distribution and quantitation.

The distribution, and quantity of immunoglobulins on the surface of lymphocytes has been studied by means of immunofluorescence and a quantitative radio-immunoassay. Surface immunoglobulins were found on approximately 45% of spleen and marrow lymphocytes and 7-14% of lymphocytes from lymph nodes, peripheral blood, and peritoneal exudate. Thymic lymphocytes contained undetectable amounts of immunoglobulin. In the spleen the different immunoglobulins were present in the following order: gammaG2 > gammaG1 > M > gammaA > gammaG3. The surface immunoglobulin was largely removable by brief treatment with trypsin. Quantitative analysis indicated that 50,000-150,000 molecules of immunoglobulin were present on an individual cell. A variety of observations make it likely that this lymphocyte-associated immunoglobulin. is a product of the cell to which it is attached rather than a form of cytophilic antibody.

Fluorescent Antibody Technique

Immunoglobulins on the surface of lymphocytes. IV. Distribution in hypogammaglobulinemia, cellular immune deficiency, and chronic lymphatic leukemia.

The distribution of peripheral blood lymphocytes that contain surface Ig has been studied by means of immunofluorescence in humans. Normal individuals, individuals with sex-linked and acquired agammaglobulinemia, selective IgA deficiency, cellular immune deficiencies, and individuals with chronic lymphatic leukemia (CLL) were studied. Approximately 28% of the peripheral blood lymphocytes from normal individuals contained surface Ig. On an average 15% contained IgG, 6%, IgA, and 8%, IgM; and the kappa: lambda ratio was 2:1. Lymphocytes from patients with CLL appeared to be "monoclonal" in that the cells from a given individual had a single Ig associated with them (e.g., kappa IgM). In three-quarters of the cases the H chain class was IgM; in the remaining one-quarter no H chain could be detected on the cell surface. The L chain class was kappa in 12 cases and lambda in 8. Four patients with sex-linked agammaglobulinemia and one with "acquired" agammaglobulinemia had markedly decreased numbers of cells with surface Ig (0-4%). In contrast, the three patients with selective IgA deficiency and no detectable serum IgA contained normal numbers of cells (6-8%) with surface IgA. Five patients with cellular deficiency states, including two with Wiskott-Aldrich syndrome, contained a normal or low percentage of cells with surface Ig.

Adolescent