Journal
PLOS ONE
Volume 3, Issue 4, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0001914
Keywords
-
Categories
Funding
- Davis-Bremer Medical Research Grant
- [K23 RR019544-01A2]
- [T32 HL07946-01]
- [RO-1HL68003]
- [RO-1HL 66108]
- [RO-1HL67176]
- [RO-1 HL63800]
- [PO-1 HL70294-02]
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Latency Associated Peptide (LAP) binds TGF-beta 1, forming a latent complex. Currently, LAP is presumed to function only as a sequestering agent for active TGF-beta 1. Previous work shows that LAP can induce epithelial cell migration, but effects on leukocytes have not been reported. Because of the multiplicity of immunologic processes in which TGF-beta 1 plays a role, we hypothesized that LAP could function independently to modulate immune responses. In separate experiments we found that LAP promoted chemotaxis of human monocytes and blocked inflammation in vivo in a murine model of the delayed-type hypersensitivity response (DTHR). These effects did not involve TGF-beta 1 activity. Further studies revealed that disruption of specific LAP-thrombospondin-1 (TSP-1) interactions prevented LAP-induced responses. The effect of LAP on DTH inhibition depended on IL-10. These data support a novel role for LAP in regulating monocyte trafficking and immune modulation.
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