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Determination of Lymphocyte JAM-C Expression in Patients With Psoriasis Vulgaris

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ClinicalTrials.gov Identifier: NCT00365625
Recruitment Status : Unknown
Verified August 2009 by Johann Wolfgang Goethe University Hospital.
Recruitment status was:  Recruiting
First Posted : August 17, 2006
Last Update Posted : February 2, 2010
Sponsor:
Information provided by:

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Recent unpublished work from our laboratory showed, that JAM-C expression of lymphocytes can be up-regulated through specific activators.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


Condition or disease
Psoriasis Psoriasis Vulgaris

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.


Study Design

Study Type : Observational
Estimated Enrollment : 30 participants
Time Perspective: Prospective
Official Title: Patient Orientated Basic Science Investigation: Determination of Lymphocyte JAM-C Expression in Patients With Psoriasis Vulgaris
Study Start Date : July 2005
Estimated Study Completion Date : December 2007

Resource links provided by the National Library of Medicine

MedlinePlus related topics: Psoriasis
U.S. FDA Resources

Groups and Cohorts


Outcome Measures

Eligibility Criteria

Information from the National Library of Medicine

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Ages Eligible for Study:   18 Years and older   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population
psoriasis patients
Criteria

Inclusion Criteria:

  • Psoriasis vulgaris
  • PASI >/= 10 at inclusion

Exclusion Criteria:

  • Psoriasis arthritis
  • Psoriasis pustulosa
  • Psoriasis palmoplantaris
  • Pregnancy
  • current infectious disease
Contacts and Locations

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): 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
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 Hospital
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:

Responsible Party: Prof. Ralf Ludwig, Johann Wolfgang Goethe University Hospitals
ClinicalTrials.gov Identifier: NCT00365625     History of Changes
Other Study ID Numbers: 244/06
First Posted: August 17, 2006    Key Record Dates
Last Update Posted: February 2, 2010
Last Verified: August 2009

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

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