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W Timens

Publications and source records attributed to W Timens.

120 records · Page 7Linked to original sources
PubMed1987

Fetal and neonatal development of human spleen: an immunohistological study.

Localization and immunophenotype of lymphocyte subsets in fetal human spleens were studied by employing a panel of monoclonal antibodies (McAb) in an immunoperoxidase staining procedure on frozen tissue sections. Spleens varied from 15 weeks of gestational age (gestational weeks, gw) to newborn. The white pulp consisted of intermediate-sized lymphocytes; no separate compartments could be discerned. Germinal centre development was not observed. Dendritic cells stained for B2, HB5, aC3bR, anti-DRC and OKIa, but in most cases not for immunoglobulin. Although low cellular immunity is observed in neonates, T cells showed adult phenotypes in proportions comparable to the adult situation; immature OKT6(+) lymphocytes were rarely seen. Very few cells stained with anti-NK cell antibody Leu7. B cells all expressed B1, Leu14, aC3bR, T10 and OKIa, were strongly positive for BA1, and mostly stained very weakly for B2 and HB5. Almost all B cells expressed IgM and IgD simultaneously, and very few expressed IgG. IgA-positive cells were absent. At 15 gw a considerable number of IgM(+) B cells showed Leu1 staining, but this decreased during development. These cells may represent the normal counterpart of Leu1(+) IgM(+) cells observed in B-CLL and immunocytic and centrocytic malignant lymphomas. After 25 gw only very few Leu1(+) IgM(+) cells were seen. Altogether, the morphology and immunophenotype of white pulp B cells were different from the predominating adult B-cell subsets, at least until birth. These 'immature' splenic B cells may be precursors for adult splenic B-cell subsets. Considering the presumed role of the marginal zone in the immunity against TI-2 antigens, the absence of a marginal zone at birth may be a main factor in the defective immunity against these antigens in neonates.

B-Lymphocytes↗
PubMed1987

Clonal immunoglobulin gene rearrangements in tissues involved by Hodgkin's disease.

The nature of Reed-Sternberg cells, the abnormal cells of Hodgkin's disease, is controversial. Morphological and immunologic marker studies suggested different cells of origin. To investigate a possible B or T cell origin, immunoglobulin and T cell receptor gene analyses were performed on tissues from 11 patients in early and late stages of Hodgkin's disease. In addition, the immunologic marker patterns of the Reed-Sternberg cells were determined. Rearrangements of immunoglobulin heavy- and light-chain genes were detected in tissues from five patients, particularly in late stages of the disease when lymphocyte depletion had occurred. No rearrangements of T cell receptor genes were found. The results indicate that clonal immunoglobulin gene rearrangements can be detected in tissues involved by Hodgkin's disease.

Adolescent↗
PubMed1986

Nodular lymphocyte predominance type of Hodgkin's disease is a germinal center lymphoma.

Nodular lymphocyte predominance type of Hodgkin's disease can be distinguished from other subtypes of Hodgkin's disease on morphological and clinical grounds. Immunohistological studies on frozen tissue sections of seven cases of nodular lymphocyte predominance type of Hodgkin's disease (NLPHD) show differences in B cell, T cell, as well as dendritic cell population. NLPHD is confined to follicles which contain predominantly small lymphocytes, usually over 50% B cells and large numbers of B2+, anti-C3b+, anti-DRC+, and Ig- dendritic cells. The IgM+, IgD+, Leu8- B lymphocytes are of polyclonal origin. The T lymphocytes in these follicles are reactive with Leu7 in addition to T11, Leu1, T3, Leu3, and WT1. Leu7 is a monoclonal antibody reactive with natural killer cells, but also with a subpopulation of Leu3+ lymphocytes present in normal germinal centers. The population with this phenotype, not found in other types of Hodgkin's disease, appears to be greatly increased (up to 30%) in NLPHD. The so-called L&H type Sternberg-Reed (S-R) cells of NLPHD are transformed B cells, reactive with anti-B cell monoclonal antibodies which in some cases express detectable amounts of membrane and/or cytoplasmic immunoglobulin. Also, L&H type Sternberg-Reed cells in all cases stained for Ki-1 and Tac, and in three cases for LeuM1. Taken together, the findings indicate that NLPHD represents a proliferation of germinal center cells.

Antibodies, Monoclonal↗
PubMed1985

Lymphocyte compartments in human spleen. An immunohistologic study in normal spleens and uninvolved spleens in Hodgkin's disease.

A panel of monoclonal antibodies directed against T and B lymphocyte antigens was used to analyze the presence and localization of several lymphocyte subsets in 13 normal human spleens (3 of newborns) and 17 uninvolved spleens of patients with Hodgkin's disease. The distribution of cells in the white pulp corresponded with findings in other secondary lymphoid organs, except for the presence of a marginal zone, a unique compartment localized at the border of white and red pulp. The phenotype of the marginal zone cells indicates that it is likely that the marginal zone contains nonrecirculating as well as recirculating B cells, while T cells (of the T helper type) are also represented. Therefore, the notion that marginal zone cells are nonrecirculating IgM+, IgD- cells, appears to be an oversimplification. No clear differences were observed between spleens of patients with and without Hodgkin's disease.

Adolescent↗
PubMed1982

Morphometrical analysis of T- and B-cell compartments of spleens in Hodgkin's disease.

One possible explanation for the defective cellular immunity in Hodgkin's disease is an abnormal distribution of T lymphocytes. To study this possibility a morphometric analysis of T- and B-areas in non involved and involved spleens of patients with Hodgkin's disease was undertaken. We found that in involved spleens a significant reduction of the T dependent area could be demonstrated. We concluded that this reduction is caused by an abnormal distribution of T lymphocytes in the spleen and may partly explain the defects in cellular immunity. In addition, the absence of overlap between the T/B area ratios of involved and non-involved spleens suggests, that a prediction on involvement of spleen can be made by morphometrical analysis of a small, random taken non-involved area.

Adolescent↗
PubMedDate not supplied

CD21.

Explore the source record for details and available documents.

Amino Acid Sequence↗
PubMedDate not supplied

Pulmonary vasculitis may obscure large cell lung carcinoma. A case report.

Several vasculitic syndromes are recognized as paraneoplastic syndromes of an underlying malignant disease. Most frequently small vessel vasculitis of the skin has been reported. We describe the case of a 62-year-old man with a pulmonary mass due to pulmonary vasculitis. After resection of the pulmonary mass, the patient displayed bone metastasis. Retrospectively, tumor cells were found in the pulmonary mass that had been resected 9 months before. In this case report the rare association of vasculitis and lung carcinoma is reviewed. Our report indicates that pulmonary vasculitis may obscure the histologic findings of lung carcinoma and that in patients with localized pulmonary vasculitis special attention has to be paid to the possible presence of malignant cells.

Carcinoma, Large Cell↗
PubMedDate not supplied

Effects of c-myc oncogene modulation on differentiation of human small cell lung carcinoma cell lines.

Amplification and over-expression of oncogenes of the myc family are related to the prognosis of certain solid tumors such as small cell lung cancer (SCLC). For SCLC, c-myc is the oncogene most consistently found to correlate with the end stage behaviour of the tumour, in particular with survival after chemotherapeutic treatment. C-myc is important in many cellular processes such as proliferation, differentiation and apoptosis. In the present study the relationship between c-myc and differentiation was analyzed by down-regulation of endogenous c-myc protein, using two approaches: first by coculturing with antisense (AS) oligodeoxynucleotides (ODN) in the human SCLC cell line GLC4 and its 6-fold cisplatin resistant subline GLC4-CDDP, second by stable transfection of GLC4-CDDP with a dexamethasone-inducible AS c-myc expression vector. Basic characterization of the differentiation status of GLC4 and GLC4-CDDP showed a decrease in neuroendocrine differentiation in GLC4-CDDP compared to GLC4 Cytokeratin was absent in both cell lines. No significant differences in expression of adhesion molecules or myeloid antigens were observed between the lines. Vimentin expression was higher in GLC4-CDDP compared to GLC4 (AS c-myc ODN)-induced growth inhibition and down-regulation of endogenous c-myc protein further decreased neuroendocrine differentiation (CD57 positive cells) in GLC4-CDDP without affecting the expression of other antigens such as vimentin (intermediate filament),CD15 (myeloid antigen) and VLA-alpha 4 (adhesion molecule) and did not alter the expression of these antigens in GLC4 (AS c-myc RNA)-induced growth inhibition did not significantly affect the expression of the tested antigens in the AS c-myc transfected GLC4-CDDP/AS cell line. No effect of nonsense c-myc ODN or dexamethasone-induced control RNA (controls) was observed.

Antigens, Differentiation↗