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Titolo:
Autocrine transforming growth factor-beta from chronic lymphocytic leukemia-B cells interferes with proliferative T cell signals
Autore:
Schuler, M; Tretter, T; Schneller, F; Huber, C; Peschel, C;
Indirizzi:
Univ Mainz, Dept Med 3, D-6500 Mainz, Germany Univ Mainz Mainz Germany D-6500 Mainz, Dept Med 3, D-6500 Mainz, Germany Tech Univ Munich, Dept Med 3, D-8000 Munich, Germany Tech Univ Munich Munich Germany D-8000 ept Med 3, D-8000 Munich, Germany
Titolo Testata:
IMMUNOBIOLOGY
fascicolo: 1, volume: 200, anno: 1999,
pagine: 128 - 139
SICI:
0171-2985(199902)200:1<128:ATGFFC>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
CD40 LIGAND; APOPTOSIS; PRECURSORS; EXPRESSION; RELEASE; DEATH; MICE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Schuler, M LanJolla Inst Allergy & Immunol, Div Cellular Immunol, 10355 Sci Ctr Dr, Sa La Jolla Inst Allergy & Immunol 10355 Sci Ctr Dr San Diego CA USA 92121
Citazione:
M. Schuler et al., "Autocrine transforming growth factor-beta from chronic lymphocytic leukemia-B cells interferes with proliferative T cell signals", IMMUNOBIOL, 200(1), 1999, pp. 128-139

Abstract

Chronic lymphocytic leukemia (CLL) is characterized by the accumulation ofnoncycling B cells in lymphatic and extralymphatic tissues. In the presentstudy we investigated the possible contribution of TGF-beta, as secreted by CLL-B cells, on this low proliferative state. CLL-B cells were shown to express TGF-beta RNA and to release bioactive TGF-beta into culture supernatants. Antibody neutralization of endogenously secreted TGF-beta increased the proliferation of CLL-B cells as cultured in the presence of IL-2 or IL-4or in direct contact with activated CD4(+) T cells. In these culture systems, addition of exogenous TGF-beta downregulated basal and cytokine-inducedproliferation of CLL-B cells. In contrast, neither neutralization of endogeneous TGF-beta, nor addition of exogeneous TGF-beta changed the proliferation of CLL-B cells as cultured in the CD40 system. In order to further explore this differential antiproliferative effect of TGF-beta, cytokine secretion of B cells and of CD4(+) T cells as well as surface marker expression of CD4(+) T cells were assessed in relation to TGF-beta: There was no negative effect of TGF-beta on autocrine secretion of TNF-alpha or sCD23 by CLL-Bcells. Unlike tonsillar B cells, CLL-B cells cultured alone or in the CD40system did no release significant amounts of IL-6 or IL-8 into supernatants. Secretion of IL-2 or IL-4 by activated CD4(+) T cells was higher, when Tcells were cocultured with normal tonsillar B cells than with CLL-B cells. The amount of IL-2 or IL-4 released by CD4(+) T cells cocultured in directcontact with tonsillar or CLL-B cells was not consistently influenced either by neutralization of endogenous TGF-beta or by addition of TGF-beta. Exogenous TGF-beta did not downregulate expression of CD40L, CD27, CD28, CD54 or mTNF-alpha by T helper cells activated with anti-CD3 or PHA. In conclusion, autocrine secretion of TGF-beta exhibits an antiproliferative effect on CLL-B cells. This effect is most relevant in B cells cultured in direct contact with activated CD4(+) T cells suggesting an indirect modeof action.

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Documento generato il 15/07/20 alle ore 21:09:08