Effect of Anti-CD303 Antibodies in Autoimmune Diseases

NCT ID: NCT03370627

Last Updated: 2020-08-27

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Clinical Phase

NA

Total Enrollment

138 participants

Study Classification

INTERVENTIONAL

Study Start Date

2017-12-20

Study Completion Date

2019-05-25

Brief Summary

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The pathogenic role of type I interferons (IFNs) in the development of different autoimmune diseases has been extensively described in the literature. Since plasmacytoid dendritic cells (pDCs) are the main source of type I IFNs, there is evidence of the involvement of pDCs in autoimmune diseases. The CD303 surface protein (also called BDCA-2) is specifically expressed by the pDCs.

The hypothesis leading to the realization of this study is to observe, in vitro, an inhibition of the secretion of the type I IFNs by pDCs in the peripheral blood in patients with autoimmune disease, thanks to the action of the anti-CD303 antibody Developed by the LFB Group, which could reduce the inflammatory response and improve patients with autoimmune disease

Detailed Description

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Conditions

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Immune Disease

Study Design

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Allocation Method

NA

Intervention Model

SINGLE_GROUP

Primary Study Purpose

BASIC_SCIENCE

Blinding Strategy

NONE

Study Groups

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Patient

Group Type EXPERIMENTAL

Monoclonal anti-cd303 antibody

Intervention Type BIOLOGICAL

Addition of monoclonal anti CD303 antibodies or not (control) on 2 blood samples of the same patient, to which 10 μl of CpG (20 μg / ml) are added in order to activate plasmacytoid Dendritic Cells and to induce the secretion of Type I interferons.

Interventions

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Monoclonal anti-cd303 antibody

Addition of monoclonal anti CD303 antibodies or not (control) on 2 blood samples of the same patient, to which 10 μl of CpG (20 μg / ml) are added in order to activate plasmacytoid Dendritic Cells and to induce the secretion of Type I interferons.

Intervention Type BIOLOGICAL

Eligibility Criteria

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Inclusion Criteria

* Have the ability to understand the requirements of the study, provide written informed consent, and comply with the study data collection procedures
* Patient followed in the department of internal medicine of CHU Lille
* Patient with one of the following autoimmune disease, defined according to international criteria: systemic lupus erythematosus, systemic sclerosis, Gougerot-Sjögren syndrome and idiopathic thrombocytopenic purpura
* Being socially insured

Exclusion Criteria

* Overlapping syndrome with another autoimmune disease
* Age ≤18 years
* Pregnant or nursing women
* People in emergencies
* Person incapable of consent
* Persons deprived of liberty
* Persons without social security cover
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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Laboratoire français de Fractionnement et de Biotechnologies

INDUSTRY

Sponsor Role collaborator

University Hospital, Lille

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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David Launay, MD,PhD

Role: PRINCIPAL_INVESTIGATOR

University Hospital, Lille

Locations

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Hôpital Claude Huriez, CHU

Lille, , France

Site Status

Countries

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France

Other Identifiers

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2017_A02244-49

Identifier Type: OTHER

Identifier Source: secondary_id

2017_23

Identifier Type: -

Identifier Source: org_study_id

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