Psoriasis Clinical Trial
Official title:
Patient Orientated Basic Science Investigation: Determination of Lymphocyte JAM-C Expression in Patients With Psoriasis Vulgaris
The stepwise process of leukocyte extravasation to inflamed tissues depends on the
expression of a variety of cytokines and adhesion molecules. Recently much attention has
focused on the Junctional Adhesion Molecules (JAM). The three members of this adhesion
molecule family, namely, JAM-A, -B and -C, have been shown to govern the last step of
leukocyte extravasation (transmigration) - the process of leukocytes passing between
endothelial cells. In addition to transmigration, some members of this family seem to
support additional steps in the leukocyte extravasation cascade. The investigators recently
showed, that antibody-mediated inhibition of JAM-C significantly reduced hapten induced skin
inflammation (J Invest Dermatol;125(5):969).
Recent unpublished work from our laboratory showed, that JAM-C expression of lymphocytes can
be up-regulated through specific activators. Hence, the investigators hypothesize, that
JAM-C expression is elevated in patients with psoriasis. As it is currently not know, which
factors may influence the expression of JAM-C, the investigators intend to analyse JAM-C
expression on CD3+CD41- cells at several time-points during the treatment of psoriatic
patients. Expression of JAM-C will then be correlated to disease activity (PASI).
Status | Recruiting |
Enrollment | 30 |
Est. completion date | December 2007 |
Est. primary completion date | |
Accepts healthy volunteers | No |
Gender | Both |
Age group | 18 Years and older |
Eligibility |
Inclusion Criteria: - Psoriasis vulgaris - PASI >/= 10 at inclusion Exclusion Criteria: - Psoriasis arthritis - Psoriasis pustulosa - Psoriasis palmoplantaris - Pregnancy - current infectious disease |
Time Perspective: Prospective
Country | Name | City | State |
---|---|---|---|
Germany | Department of Dermatology - Clinic of the Johann Wolfgang Goethe University | Frankfurt Am Main | Hessen |
Lead Sponsor | Collaborator |
---|---|
Johann Wolfgang Goethe University Hospitals |
Germany,
Aurrand-Lions M, Lamagna C, Dangerfield JP, Wang S, Herrera P, Nourshargh S, Imhof BA. Junctional adhesion molecule-C regulates the early influx of leukocytes into tissues during inflammation. J Immunol. 2005 May 15;174(10):6406-15. — View Citation
Chavakis T, Keiper T, Matz-Westphal R, Hersemeyer K, Sachs UJ, Nawroth PP, Preissner KT, Santoso S. The junctional adhesion molecule-C promotes neutrophil transendothelial migration in vitro and in vivo. J Biol Chem. 2004 Dec 31;279(53):55602-8. Epub 2004 Oct 14. — View Citation
Lamagna C, Hodivala-Dilke KM, Imhof BA, Aurrand-Lions M. Antibody against junctional adhesion molecule-C inhibits angiogenesis and tumor growth. Cancer Res. 2005 Jul 1;65(13):5703-10. — View Citation
Ludwig RJ, Zollner TM, Santoso S, Hardt K, Gille J, Baatz H, Johann PS, Pfeffer J, Radeke HH, Schön MP, Kaufmann R, Boehncke WH, Podda M. Junctional adhesion molecules (JAM)-B and -C contribute to leukocyte extravasation to the skin and mediate cutaneous inflammation. J Invest Dermatol. 2005 Nov;125(5):969-76. — View Citation
Muller WA. Leukocyte-endothelial-cell interactions in leukocyte transmigration and the inflammatory response. Trends Immunol. 2003 Jun;24(6):327-34. Review. — View Citation
Santoso S, Orlova VV, Song K, Sachs UJ, Andrei-Selmer CL, Chavakis T. The homophilic binding of junctional adhesion molecule-C mediates tumor cell-endothelial cell interactions. J Biol Chem. 2005 Oct 28;280(43):36326-33. Epub 2005 Aug 23. — View Citation
Santoso S, Sachs UJ, Kroll H, Linder M, Ruf A, Preissner KT, Chavakis T. The junctional adhesion molecule 3 (JAM-3) on human platelets is a counterreceptor for the leukocyte integrin Mac-1. J Exp Med. 2002 Sep 2;196(5):679-91. — View Citation
Vonlaufen A, Aurrand-Lions M, Pastor CM, Lamagna C, Hadengue A, Imhof BA, Frossard JL. The role of junctional adhesion molecule C (JAM-C) in acute pancreatitis. J Pathol. 2006 Aug;209(4):540-8. — View Citation
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