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Clinical Trial Details — Status: Recruiting

Administrative data

NCT number NCT00365625
Other study ID # 244/06
Secondary ID
Status Recruiting
Phase N/A
First received August 16, 2006
Last updated February 1, 2010
Start date July 2005
Est. completion date December 2007

Study information

Verified date August 2009
Source Johann Wolfgang Goethe University Hospitals
Contact Ralf J Ludwig, MD
Phone 0049-69-6301-
Email r.ludwig@em.uni-frankfurt.de
Is FDA regulated No
Health authority Germany: Ethics Commission
Study type Observational

Clinical Trial Summary

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Recent unpublished work from our laboratory showed, that JAM-C expression of lymphocytes can be up-regulated through specific activators.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).


Description:

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. We 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, we 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, we 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).

Detailed in- and exclusion criteria are outlined below.


Recruitment information / eligibility

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

Study Design

Time Perspective: Prospective


Related Conditions & MeSH terms


Locations

Country Name City State
Germany Department of Dermatology - Clinic of the Johann Wolfgang Goethe University Frankfurt Am Main Hessen

Sponsors (1)

Lead Sponsor Collaborator
Johann Wolfgang Goethe University Hospitals

Country where clinical trial is conducted

Germany, 

References & Publications (8)

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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