Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.24.59 (
MIP
)
4,906
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Interleukin 13
(
IL-13
) is a recently described protein secreted by activated T cells and is a potent in vitro modulator of human monocyte and B-cell functions.
IL-13
shares some biologic properties as well as structural similarities with IL-4. Macrophage-inflammatory protein 1 alpha (
MIP
-1 alpha) is a product of activated monocytes and macrophages and an important activator of T cells, monocytes, and macrophages. We determined the effect of human recombinant
IL-13
on lipopolysaccharide (LPS)- and IL-1 beta-induced
MIP
-1 alpha mRNA and protein expression from peripheral blood monocytes (PBM) and alveolar macrophages (AM). In PBM, basal
MIP
-1 alpha protein was 20 +/- 7 pM and increased following LPS and IL-1 beta to 1,520 +/- 193 (P < 0.001) and 233 +/- 50 (P < 0.003) pM.
IL-13
(25 ng/ml) reduced these values by 55 +/- 10% [not significant (NS)], 43 +/- 9% (P < 0.03), and 44 +/- 15% (NS), respectively. LPS- and IL-1 beta-induced
MIP
-1 alpha mRNA expression was reduced by 43 +/- 5% (P < 0.01) and 41 +/- 4% (NS). In AM,
IL-13
reduced LPS-induced
MIP
-1 alpha protein release of 2,030 +/- 242 pM by 32 +/- 8% (P < 0.05) and
MIP
-1 alpha mRNA by 27 +/- 1% (NS). For both PBM and AM, the inhibitory effect of
IL-13
on
MIP
-1 alpha protein was maximal at 24 h, was dose dependent with a maximal effect at 100 ng/ml, and was similar to, although slightly less potent than, that seen with IL-4. In PBM, the inhibitory effect of
IL-13
required de novo protein synthesis and was not due to enhanced mRNA decay. Thus,
IL-13
has inhibitory effects on the transcription of
MIP
-1 alpha from monocytes and macrophages, and as is the case with IL-4 and IL-10, may be an important mediator for suppressing inflammatory responses.
...
PMID:Interleukin 13 inhibits macrophage inflammatory protein-1 alpha production from human alveolar macrophages and monocytes. 881 Jun 43