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Query: UNIPROT:Q06643 (
non-Hodgkin's lymphoma
)
11,307
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A 56-year-old man with refractory B-cell lymphocytic
non-Hodgkin's lymphoma
was treated in a Phase II study with interleukin-2 (IL-2) (Roussel-Uclaf, Romainville, France). The patient had involvement of multiple lymph nodes and medullary and peripheral blood (3.6 x 10(9) monoclonal CD19-positive [CD19+] B-lymphocytes/l). After a 5-day cycle of IL-2 treatment, an eightfold increase of the monoclonal CD19+ population was observed (27 x 10(9) monoclonal CD19+ cells). The lymphocytosis decreased dramatically during the second cycle (days 15 to 19) of IL-2 treatment, resulting in 6 x 10(9)/l peripheral lymphocytes, with 5.5 x 10(9) B-lymphocytes. As soon as day 20, peripheral B-cells again increased considerably, with 32 x 10(9) CD19+ cells/l at day 27. The CD19+ population remained monoclonal as assessed by kappa/lambda cell-surface phenotyping and kappa gene rearrangement evaluation. Kinetics of the monoclonal B-lymphocyte response to IL-2 paralleled the natural killer/lymphokine-activated killer and T-cell response, with a 4-day latency period, suggesting an indirect enhancing effect of IL-2. Before and during IL-2 treatment, peripheral B-lymphocytes never expressed detectable levels of the p55 IL-2 receptor. However, the p75 IL-2 receptor was expressed significantly in the IL-2-responsive monoclonal B-cell population.
Tumor necrosis factor alpha
, a known (in vitro) B-cell tumor growth factor, reached high serum levels during IL-2 treatment. Response evaluation at day 45 showed stability of the lymph node involvement and the marrow lymphocyte infiltrate. At day 45, peripheral B-cell lymphocytosis was 7.5 x 10(9)/l. To the knowledge of the authors, this is the first report of an in vivo IL-2-induced reversible increase of peripheral monoclonal B-cell lymphocytosis.
...
PMID:Interleukin-2-induced increase of a monoclonal B-cell lymphocytosis. A novel in vivo interleukin-2 effect? 156 83
Tumor necrosis factor alpha
(
TNF-alpha
) and soluble lymphotoxin (LT) (also called LT-alpha or TNF-beta) are cytokines with similar biological activities that are encoded by related and closely linked genes.
TNF-alpha
, a mediator of the inflammatory response, exists in soluble and transmembrane forms. LT-alpha can be secreted or retained at the cell surface by binding to a 33-kDa transmembrane subunit,
LT-beta
. The recently cloned human
LT-beta
gene encodes another TNF family member and is linked to the TNF/LT locus within the major histocompatibility complex locus. The cell surface LT is a heterotrimer consisting of LT-alpha and
LT-beta
, whose physiological function is not yet clearly defined. We now report the sequence analysis of the genomic region and cDNA of murine
LT-beta
gene, which is closely associated with the
TNF-alpha
and LT-alpha genes within the murine major histocompatibility complex locus. Unlike the
TNF-alpha
, LT-alpha, and human
LT-beta
genes, which contain four exons, the murine
LT-beta
contains three exons and encodes a 244-amino acid polypeptide with a 66-amino acid insert that is absent from the human homologue. In situ hybridization demonstrates constitutive expression of
LT-beta
in lymphoid and hematopoietic tissues.
LT-beta
transcription is maximal in the thymic medulla and in splenic white pulp.
LT-beta
mRNA is also detected in the skin and in specific regions of the brain. The
LT-beta
promoter region contains putative Ets-binding sites, suggesting that the expression of
LT-beta
may be regulated in part by Ets transcription factors whose pattern of lymphoid expression overlaps that of
LT-beta
.
...
PMID:Cloning and expression analysis of the murine lymphotoxin beta gene. 784 35
Tumor necrosis factor alpha
(TNF alpha) is a pleiotropic cytokine that is constitutively produced by leukemic cells in B Chronic Lymphocytic Leukemia (B-CLL). It has been shown to have autocrine and paracrine functions in normal B cells and in B lymphoproliferative diseases. This study was conducted to determine the effect of TNF alpha (in vitro) on CD20 expression on cells from patients with B-CLL. Currently, anti-CD20 monoclonal antibody therapy is becoming a second line treatment in the management of B cell disorders like low-grade
non-Hodgkin's lymphoma
(
NHL
) and B-CLL. Our results demonstrate amply that very low doses of TNF alpha (0. 0125 ng/ml) can be used to significantly increase CD20 expression on cells from patients of B-CLL as evidenced by increases in both percentage positivity and mean fluorescence intensity. The upregulation is evident as early as 24 hours and is maintained for up to 72 hours. We propose that the upregulation is a direct result of in vitro differentiation stimulated by TNF alpha. The results presented can be exploited in the designing of priming protocols prior to antibody therapy and this is discussed.
...
PMID:Tumor necrosis factor modulates CD 20 expression on cells from chronic lymphocytic leukemia: a new role for TNF alpha? 1089 91