PsoriasisNCT00365625
Determination of Lymphocyte JAM-C Expression in Patients With Psoriasis Vulgaris
An observational study of Psoriasis and Psoriasis Vulgaris, run by Johann Wolfgang Goethe University Hospital at 1 site in Germany.
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). Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Psoriasis, Psoriasis Vulgaris
- How many people
- 30 participants
- Where
- 1 siteGermany
- Study dates
- Jul 2005to Dec 2007
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: psoriasis patients
Who may be able to join
- Psoriasis vulgaris
- PASI >/= 10 at inclusion
Who cannot join
- Psoriasis arthritis
- Psoriasis pustulosa
- Psoriasis palmoplantaris
- Pregnancy
- current infectious disease
Trial locations and contacts
1 site in 1 country.
Germany1 site, 1 recruiting
- Recruiting
Department of Dermatology - Clinic of the Johann Wolfgang Goethe University
Frankfurt am Main, Hesse, 60590
Ralf J Ludwig, MD, 0049-69-6301- ext. 6162, r.ludwig@em.uni-frankfurt.de
Wolf-Henning Boehncke, Professor, 0049-69-6301- ext. 5743, boehncke@em.uni-frankfurt.de
About this study
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).
Read the 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.
- Conditions
- Psoriasis, Psoriasis Vulgaris
- Keywords
- Psoriasis, JAM3 protein, human, Cell Adhesion Molecules, Skin, Inflammation, Lymphocytes
- Medical subject headings
- Psoriasis, Inflammation
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted17 Aug 2006 (estimated)
- Study startJul 2005
- Study completionDec 2007 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (8)Papers the sponsor has linked to this study.
- Other trials for PsoriasisStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Time perspective
- Prospective
- Enrolment
- 30 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Johann Wolfgang Goethe University Hospital
- Sponsor type
- University, hospital or other
- Investigators
- Ralf J Ludwig, MD, Principal investigator, Department of Dermatology - Clinic of the Johann Wolfgang Goethe UniversityRoland Kaufmann, Professor, Study chair, Department of Dermatology - Clinic of the Johann Wolfgang Goethe UniversityWolf-Henning Boehncke, Professor, Study chair, Department of Dermatology - Clinic of the Johann Wolfgang Goethe University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00365625
- Sponsor's protocol ID
- 244/06
- Status last verified
- Aug 2009
- First submitted
- 16 Aug 2006
- Last updated
- 2 Feb 2010
- Results posted
- No
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. doi: 10.1111/j.0022-202X.2005.23912.x.
PubMed 16297198Santoso 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. doi: 10.1084/jem.20020267.
PubMed 12208882Chavakis 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. doi: 10.1074/jbc.M404676200. Epub 2004 Oct 14.
PubMed 15485832Muller WA. Leukocyte-endothelial-cell interactions in leukocyte transmigration and the inflammatory response. Trends Immunol. 2003 Jun;24(6):327-34. doi: 10.1016/s1471-4906(03)00117-0.
PubMed 12810109Vonlaufen 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. doi: 10.1002/path.2007.
PubMed 16767690Santoso 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. doi: 10.1074/jbc.M505059200. Epub 2005 Aug 23.
PubMed 16118203Lamagna 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. doi: 10.1158/0008-5472.CAN-04-4012.
PubMed 15994945Aurrand-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. doi: 10.4049/jimmunol.174.10.6406.
PubMed 15879142
Study at a glance
From the registry record, last updated by the sponsor on 2 Feb 2010. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Patient Orientated Basic Science Investigation: Determination of Lymphocyte JAM-C Expression in Patients With Psoriasis Vulgaris
- ClinicalTrials.gov ID
- NCT00365625
- Acronym / sponsor ID
- 244/06
- Conditions
- Psoriasis, Psoriasis Vulgaris
- Keywords
- Psoriasis, JAM3 protein, human, Cell Adhesion Molecules, Skin, Inflammation, Lymphocytes
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 30 participants (estimated)
- Lead sponsor
- Johann Wolfgang Goethe University HospitalUniversity, hospital or other
- Study start
- Jul 2005
- Study completion
- Dec 2007 (estimated)
- First posted
- 17 Aug 2006 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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).
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
- Time perspective
- Prospective
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- psoriasis patients
Key inclusion criteria (2 listed)
- Psoriasis vulgaris
- PASI >/= 10 at inclusion
Key exclusion criteria (5 listed)
- Psoriasis arthritis
- Psoriasis pustulosa
- Psoriasis palmoplantaris
- Pregnancy
- current infectious disease
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Not reported in the source record.
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 2 Feb 2010.
- Background: PubMed 16297198Ludwig 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. doi: 10.1111/j.0022-202X.2005.23912.x.
- Background: PubMed 12208882Santoso 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. doi: 10.1084/jem.20020267.
- Background: PubMed 15485832Chavakis 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. doi: 10.1074/jbc.M404676200. Epub 2004 Oct 14.
- Background: PubMed 12810109Muller WA. Leukocyte-endothelial-cell interactions in leukocyte transmigration and the inflammatory response. Trends Immunol. 2003 Jun;24(6):327-34. doi: 10.1016/s1471-4906(03)00117-0.
- Background: PubMed 16767690Vonlaufen 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. doi: 10.1002/path.2007.
- Background: PubMed 16118203Santoso 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. doi: 10.1074/jbc.M505059200. Epub 2005 Aug 23.
- Background: PubMed 15994945Lamagna 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. doi: 10.1158/0008-5472.CAN-04-4012.
- Background: PubMed 15879142Aurrand-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. doi: 10.4049/jimmunol.174.10.6406.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Ralf J Ludwig, MD principal investigator
Department of Dermatology - Clinic of the Johann Wolfgang Goethe University
Roland Kaufmann, Professor study chair
Department of Dermatology - Clinic of the Johann Wolfgang Goethe University
Wolf-Henning Boehncke, Professor study chair
Department of Dermatology - Clinic of the Johann Wolfgang Goethe University
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Psoriasis and Psoriasis Vulgaris, run by Johann Wolfgang Goethe University Hospital at 1 site in Germany.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 2 inclusion and 5 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 2 Feb 2010. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Germany. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Ralf J Ludwig, MD (0049-69-6301- ext. 6162, r.ludwig@em.uni-frankfurt.de), or a site near the patient. AzTrials does not enrol participants or take referrals.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00365625, which also lists 8 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 2 Feb 2010.