Latency associated peptide has in vitro and in vivo immune effects independent of TGF-β1

Naeem A. Ali, Alice A. Gaughan, Charles G. Orosz, Chris P. Baran, Sara McMaken, Yijie Wang, Timothy D. Eubank, Melissa Hunter, Frank J. Lichtenberger, Nicholas A. Flavahan, Jack Lawler, Clay B. Marsh

Research output: Contribution to journalArticlepeer-review


Latency Associated Peptide (LAP) binds TGF-β1, forming a latent complex Currently, LAP is presumed to function only as a sequestering agent for active TGF-β1. Previous work show that LAP can induce epithelial cell migration, but effect on leukocyte have not been reported. Because of the multiplicity of immunologic processes in which TGF-β1 plays a role, we hypothesized that LAP could function independently to modulate immune response. In separate experiments we found that LAP promoted chemotaxis opf human monocytes and blocked inflammation in vivo in a murine model of the delayed-type hypersensitivity response (DTHR). These effects did not involve TGF-B1 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.

Original languageEnglish (US)
Article numbere1914
JournalPloS one
Issue number4
StatePublished - Apr 2 2008

ASJC Scopus subject areas

  • General


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