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Titolo:
INDUCTION BY IL-9 AND SUPPRESSION BY IL-3 AND IL-4 OF THE LEVELS OF CHROMOSOME-14-DERIVED TRANSCRIPTS THAT ENCODE LATE-EXPRESSED MOUSE MAST-CELL PROTEASES
Autore:
EKLUND KK; GHILDYAL N; AUSTEN KF; STEVENS RL;
Indirizzi:
HARVARD UNIV,SCH MED,DEPT MED,SEELEY G MUDD BLDG,RM 617,250 LONGWOOD AVE BOSTON MA 02115 HARVARD UNIV,SCH MED,DEPT MED,SEELEY G MUDD BLDG,RM 617,250 LONGWOOD AVE BOSTON MA 02115 BRIGHAM & WOMENS HOSP,DEPT RHEUMATOL & IMMUNOL BOSTON MA 02115 UNIV HELSINKI,DEPT MED CHEM SF-00100 HELSINKI 10 FINLAND
Titolo Testata:
The Journal of immunology
fascicolo: 8, volume: 151, anno: 1993,
pagine: 4266 - 4273
SICI:
0022-1767(1993)151:8<4266:IBIASB>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONNECTIVE-TISSUE-TYPE; STIMULATORY FACTOR-I; GROWTH-ENHANCING ACTIVITY; C-KIT LIGAND; T-CELL; MOLECULAR-CLONING; BONE-MARROW; TRICHINELLA-SPIRALIS; SERINE PROTEASES; MESSENGER-RNA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
K.K. Eklund et al., "INDUCTION BY IL-9 AND SUPPRESSION BY IL-3 AND IL-4 OF THE LEVELS OF CHROMOSOME-14-DERIVED TRANSCRIPTS THAT ENCODE LATE-EXPRESSED MOUSE MAST-CELL PROTEASES", The Journal of immunology, 151(8), 1993, pp. 4266-4273

Abstract

Immature, rIL-3-dependent mouse bone marrow-derived mast cells (BMMC)contain high steady-state levels of the mouse mast cell protease (mMCP) 5 transcript but undetectable levels of the mMCP-1, mMCP-2, or mMCP-4 transcripts even though all four of their genes reside at a locus on chromosome 14. These mast cells can be induced by recombinant c-kit ligand (rKL) to obtain high steady-state levels of the mMCP-4 transcript and by rIL-10 to obtain high steady-state levels of the mMCP-1 and mMCP-2 transcripts. rIL-3 and rKL both elicit the differentiation of progenitor cells into immature BMMC and then stimulate their proliferation. We now report that although rIL-9 alone has no effect on BMMC proliferation as assessed by their incorporation of [H-3]thymidine, rIL-9in combination with rKL enhances the long term viability of BMMC. Furthermore, rIL-9 in the presence of rKL stimulates mouse BMMC to undergo a phenotypic change by inducing accumulation of high steady-state levels of the mMCP-1 and mMCP-2 transcripts. In contrast, in BMMC, the presence of rIL-4 suppresses the rIL-9-induced accumulation of the mMCP-1 and mMCP-2 transcripts, the rIL-10-induced accumulation of the mMCP-1 and mMCP-2 transcripts, and the rKL-induced accumulation of the mMCP-4 transcript, but not the rIL-3-induced accumulation of the mMCP-5 transcript. The presence of rIL-3 also suppresses the rIL-9-induced accumulation of the mMCP-1 and mMCP-2 transcripts. Because of their counter-regulatory, actions on the steady-state levels of transcripts that encode three late-expressed serine proteases in BALB/cJ mice, rIL-4 and rIL-3 both inhibit the final stages of differentiation and maturation of mast cells. Because rIL-4, unlike rIL-3, is neither an inducer ofearly-expressed proteases nor alone a proliferative factor for BMMC, the counterregulatory actions of rIL-3 and rIL-4 on differentiation and maturation of these mouse mast cells are independent of their other functions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 09:17:41