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Determination of Lymphocyte JAM-C Expression in Patients With Psoriasis Vulgaris
This study is currently recruiting participants.
Verified by Johann Wolfgang Goethe University Hospitals, April 2007
First Received: August 16, 2006   Last Updated: April 3, 2007   History of Changes
Sponsored by: Johann Wolfgang Goethe University Hospitals
Information provided by: Johann Wolfgang Goethe University Hospitals
ClinicalTrials.gov Identifier: NCT00365625
  Purpose

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Recent unpublished work from our laboratory showed, that JAM-C expression of lymphocytes can be up-regulated through specific activators.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


Condition
Psoriasis
Psoriasis Vulgaris

MedlinePlus related topics: Adhesions Psoriasis
U.S. FDA Resources
Study Type: Observational
Study Design: Natural History, Longitudinal, Defined Population, Prospective Study
Official Title: Patient Orientated Basic Science Investigation: Determination of Lymphocyte JAM-C Expression in Patients With Psoriasis Vulgaris

Further study details as provided by Johann Wolfgang Goethe University Hospitals:

Estimated Enrollment: 30
Study Start Date: July 2005
Estimated Study Completion Date: December 2007
Detailed 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.

  Eligibility

Ages Eligible for Study:   18 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

  • Psoriasis vulgaris
  • PASI >/= 10 at inclusion

Exclusion Criteria:

  • Psoriasis arthritis
  • Psoriasis pustulosa
  • Psoriasis palmoplantaris
  • Pregnancy
  • current infectious disease
  Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT00365625

Contacts
Contact: Ralf J Ludwig, MD 0049-69-6301- ext 6162 r.ludwig@em.uni-frankfurt.de
Contact: Wolf-Henning Boehncke, Professor 0049-69-6301- ext 5743 boehncke@em.uni-frankfurt.de

Locations
Germany, Hessen
Department of Dermatology - Clinic of the Johann Wolfgang Goethe University Recruiting
Frankfurt am Main, Hessen, Germany, 60590
Contact: Ralf J Ludwig, MD     0049-69-6301- ext 6162     r.ludwig@em.uni-frankfurt.de    
Contact: Wolf-Henning Boehncke, Professor     0049-69-6301- ext 5743     boehncke@em.uni-frankfurt.de    
Sponsors and Collaborators
Johann Wolfgang Goethe University Hospitals
Investigators
Principal Investigator: Ralf J Ludwig, MD Department of Dermatology - Clinic of the Johann Wolfgang Goethe University
Study Chair: Roland Kaufmann, Professor Department of Dermatology - Clinic of the Johann Wolfgang Goethe University
Study Chair: Wolf-Henning Boehncke, Professor Department of Dermatology - Clinic of the Johann Wolfgang Goethe University
  More Information

Additional Information:
Publications:
Ludwig RJ, Zollner TM, Santoso S, Hardt K, Gille J, Baatz H, Johann PS, Pfeffer J, Radeke HH, Schon 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.
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.
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.
Muller WA. Leukocyte-endothelial-cell interactions in leukocyte transmigration and the inflammatory response. Trends Immunol. 2003 Jun;24(6):327-34. Review.
Vonlaufen A, Aurrand-Lions M, Pastor C, Lamagna C, Hadengue A, Imhof B, Frossard JL. The role of junctional adhesion molecule C (JAM-C) in acute pancreatitis. J Pathol. 2006 Aug;209(4):540-8.
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.
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.
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.

Study ID Numbers: 244/06
Study First Received: August 16, 2006
Last Updated: April 3, 2007
ClinicalTrials.gov Identifier: NCT00365625     History of Changes
Health Authority: Germany: Ethics Commission

Keywords provided by Johann Wolfgang Goethe University Hospitals:
Psoriasis
JAM3 protein, human
Cell Adhesion Molecules
Skin
Inflammation
Lymphocytes

Study placed in the following topic categories:
Skin Diseases
Psoriasis
Adhesions
Skin Diseases, Papulosquamous
Inflammation

Additional relevant MeSH terms:
Skin Diseases
Psoriasis
Skin Diseases, Papulosquamous

ClinicalTrials.gov processed this record on May 06, 2009