MODULATION OF EXPRESSION OF THE ANTIINFLAMMATORY CYTOKINES INTERLEUKIN-13 AND INTERLEUKIN-10 BY INTERLEUKIN-3

Citation
Ev. Marietta et al., MODULATION OF EXPRESSION OF THE ANTIINFLAMMATORY CYTOKINES INTERLEUKIN-13 AND INTERLEUKIN-10 BY INTERLEUKIN-3, European Journal of Immunology, 26(1), 1996, pp. 49-56
Citations number
39
Categorie Soggetti
Immunology
ISSN journal
00142980
Volume
26
Issue
1
Year of publication
1996
Pages
49 - 56
Database
ISI
SICI code
0014-2980(1996)26:1<49:MOEOTA>2.0.ZU;2-O
Abstract
Interleukin (IL)-4, IL-10 and IL-13 are cytokines with potent anti-inf lammatory activities. Prevention of pathological inflammation at mucos al surfaces appears to be due, in part, to the presence of these cytok ines. One potential source for these cytokines is the mast cell which resides at mucosal surfaces. Demonstrated in this report are the findi ngs that bone marrow-derived mucosal-like mast cells constitutively ex pressed IL-13 whereas bone marrow-derived connective tissue-like mast cells demonstrated IL-13 transcription only after Fc epsilon RI-mediat ed activation or the addition of exogenous IL-3. A similar pattern of expression of IL-10 by these mast cell types was also evident and matc hes that of IL-4 previously reported. Intracellular cytokine staining indicated that IL-10 protein is constitutively expressed by the bone m arrow-derived mucosal-like mast cells but is only evident in the bone marrow-derived connective tissue-like mast cells after induction with IL-3. The increase of IL-13 and IL-10 transcripts in the connective ti ssue-like mast cells following IL-3 treatment is not mast cell specifi c, in that splenic and bone marrow cells also demonstrated the same ph enomenon. These data suggest that mucosal mast cells may have a consti tutive repertoire of Th2 cytokines with potential anti-inflammatory ac tivity, while connective tissue mast cells may not. However, productio n of such cytokines can be induced in the connective tissue mast cell and other cell types of the immune response by the addition of IL-3.