SarcoidosisMOSARNCT05916638
MoMa Signature During Granulomatosis
An observational study of Sarcoidosis and Tuberculosis, run by Assistance Publique - Hôpitaux de Paris at 1 site in France.
Trial summary
Sarcoidosis is a systemic inflammatory disease characterized by unspecific granuloma formation. Our hypothesis is that granuloma formation and maintenance mainly relies on the overactivation of monocytes (Mo) and macrophages (Ma). Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Sarcoidosis, Tuberculosis
- What is being tested?
- blood sample
- How many people
- 100 participants
- Where
- 1 siteFrance
- Study dates
- 15 Jan 2024to Jan 2030
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
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: Adult patients diagnosed with sarcoidosis or tuberculosis
Who may be able to join
- Male and female > 18 years old
- Diagnosis of sarcoidosis and of tuberculosis
- Affiliated to medical insurance
Who cannot join
- HIV infection
- pregnant or breastfeeding woman
- Patient under legal protection, guardianship or curators
- Absence of signed consent" Secondary exclusion criteria Other causes of granulomatosis ultimately identified as sarcoidosis or tuberculosis
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
France1 site, 1 recruiting
- Recruiting
Hôpital Bichat
Paris, 75018
Karim SACRE, MD, PhD, karim.sacre@aphp.fr
About this study
Official title: Role of Monocytes (Mo) and Macrophages (Ma) in Sarcoidosis and in Tuberculosis
Sarcoidosis is a systemic inflammatory disease characterized by unspecific granuloma formation. Our hypothesis is that granuloma formation and maintenance mainly relies on the overactivation of monocytes (Mo) and macrophages (Ma). To this end, the study aims (i) to define MoMa systemic signature in sarcoidosis, (ii) to characterize this signature in situ on tissue samples, and (iii) to identify causative factors that participate to the MoMa chronic overactivation. Thus, a cohort of sarcoidosis patients will be compared with tuberculosis patients. The MoMa systemic signature will be defined on whole blood (TruCulture model) and then in situ through different methods (multi-parameter spectral flow cytometry, RNA-seq, Luminex, imaging mass cytometry). The epigenome of monocytes will be studied thanks to CUT\&Tag. The MoMa systemic signature will be defined ex vivo at different time points during the course of the disease with phenotypic, transcriptomic, cytokine and functional approaches. The previously identified signature will be studied in situ and completed by the characterization of granuloma architecture and microenvironmental interactions, which could be modulated by epigenetic modifications. Hence, the epigenome of monocytes will be analyzed in two groups (sarcoidosis and tuberculosis). These results would allow to better understand sarcoidosis physiopathology and, in fine, may raise new therapeutic strategies. Finally, the study could challenge the dogma on innate immunity/auto-inflammation versus adaptive immunity/auto-immunity/memory.
Read the detailed description
"Sarcoidosis is an inflammatory disease characterized by the presence of coalescing, tightly clustered, non-necrotizing granulomas. The diagnosis is based on three major criteria: a compatible clinical presentation, the presence of non-necrotizing granulomatous inflammation, and the exclusion of alternative granulomatous diseases. A wide range of clinical phenotypes are observed depending on the location of the granulomatous lesions which can affect any organ, with the lungs being the most affected site. Sarcoidosis shares many similarities with tuberculosis, in which granuloma formation is triggered by Mycobacterium tuberculosis (M. tb). These phenotypic similarities between the two diseases present many challenges for diagnosis, clinical management and therapy.
Our understanding of the factors that contribute to sarcoidosis development, granuloma formation and maintenance remains limited. Part of this challenge is that granuloma development may involve both environmental and genetic factors, which contribute to the recruitment of immune cells to form the granuloma. Immune cells involved in the granuloma include (1) CD4 Th1 and Th17 T cells and their associated cytokines (e.g, IFNγ, TNFα, IL-17, IL-2); and (2) monocytes (Mo) and macrophages (Ma) including proinflammatory M1 and pro-fibrosis M2 types. However, the specific factors that contribute to granuloma maintenance and evolution remain to be identified. Among them, we can hypothesized that trained immunity, persistence of the antigen, or the microenvironment are involved in this chronic dysregulated immune response. Such an improved understanding of the pathophysiology of the disease may allow development of new treatments, as currently corticosteroids remain the mainstay of therapy.
Our main hypothesis is that granuloma formation and maintenance mainly relies on the overactivation of monocytes (Mo) and macrophages (Ma). To this end, the study aims (i) to define MoMa systemic signature in sarcoidosis, (ii) to characterize this signature in situ on tissue samples, and (iii) to identify causative factors that participate to the MoMa chronic overactivation. Thus, a cohort of sarcoidosis patients will be compared with tuberculosis patients. The MoMa systemic signature will be defined on whole blood (TruCulture model) and then in situ through different methods (multi-parameter spectral flow cytometry, RNA-seq, Luminex, imaging mass cytometry). The epigenome of monocytes will be studied thanks to CUT\&Tag. The MoMa systemic signature will be defined ex vivo at different time points (M0, M6 and M12) during the course of the disease with phenotypic, transcriptomic, cytokine and functional approaches. The previously identified signature will be studied in situ and completed by the characterization of granuloma architecture and microenvironmental interactions, which could be modulated by epigenetic modifications. Hence, the epigenome of monocytes will be analyzed in two groups (sarcoidosis and tuberculosis). These results would allow to better understand sarcoidosis physiopathology and, in fine, may raise new therapeutic strategies. Finally, the study could challenge the dogma on innate immunity/auto-inflammation versus adaptive immunity/auto-immunity/memory."
- Conditions
- Sarcoidosis, Tuberculosis
- Being tested
- blood sample
- Keywords
- tuberculosis, sarcoidosis, granuloma, monocytes, macrophages
- Medical subject headings
- Sarcoidosis, Tuberculosis, Granuloma
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
blood sampleOther
blood sample collection
| Study group | Role | What they receive |
|---|---|---|
| Sarcoidosis | patients diagnosed with sarcoidosis Receives: Other: blood sample | |
| Tuberculosis | patients diagnosed with tuberculosis Receives: Other: blood sample |
What is being measured
The primary outcome is the main question the study is designed to answer.
macrophage activation in sarcoidosis measured by epigenomic
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
Measured: up to 12 months of follow-up.
monocyte activation in sarcoidosis measured by epigenomic
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
Measured: up to 12 months of follow-up.
macrophage activation in sarcoidosis measured by spatial transcriptomics
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
Measured: up to 12 months of follow-up.
monocyte activation in sarcoidosis measured by spatial transcriptomics
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
Measured: up to 12 months of follow-up.
monocyte activation in sarcoidosis measured by transcriptomic
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
Measured: up to 12 months of follow-up.
macrophage activation in sarcoidosis measured by transcriptomic
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
Measured: up to 12 months of follow-up.
macrophage activation in sarcoidosis measured by cytokine measurement
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
Measured: up to 12 months of follow-up.
monocyte activation in sarcoidosis measured by cytokine measurement
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
Measured: up to 12 months of follow-up.
Secondary outcomes (6)
monocyte activation in tuberculosis measured by epigenomic
Measured: up to 12 months of follow-up.
Identification of a pathogen that triggers sarcoidosis development by metagenomic study
Measured: Samples collected before treatment/at diagnosis
identification of epigenetic modifications of monocytes by CUT&Tag method
CUT\&Tag-sequencing, also known as cleavage under targets and tagmentation, is a method used to analyze protein interactions with DNA
Measured: 12 months of follow-up.
Identification of a diagnostic test to discriminate sarcoidosis and tuberculosis
measurement of IFNγ secretion by whole blood in response to stimulation by tuberculosis antigen
Measured: Samples collected before treatment/at diagnosis
real-time analysis of oxidative phosphorylation of monocyte
By Seahorse methode
Measured: up to 12 months of follow-up
real-time analysis of glycolysis of monocytes
by seahorse method
Measured: up to 12 month of follow up
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted23 Jun 2023
- Study start15 Jan 2024
- Primary completionJan 2029 (estimated)
- Study completionJan 2030 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (1)Papers the sponsor has linked to this study.
- Other trials for SarcoidosisStudies of the same condition, open and under way.
- More trials run by Assistance Publique - Hôpitaux de ParisThe sponsor's other registered studies.
- 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
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 100 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Assistance Publique - Hôpitaux de Paris
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Karim SACRE, MD-PhD, PU-PH, Principal investigator, Assistance Publique - Hôpitaux de Paris
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05916638
- Sponsor's protocol ID
- APHP230273
- Other IDs
- 2022-A02637-36
- Acronym
- MOSAR
- Status last verified
- Feb 2026
- First submitted
- 17 May 2023
- Last updated
- 3 Mar 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Publications
Robert M, Boizeau L, Cappy P, Villain E, Culina S, Sannier A, Yatim N, Mageau A, Charles N, Rodriguez C, Peiffer-Smadja N, Borie R, Duffy D, Woerther PL, Sacre K. Systemic and local lymph node inflammation at disease onset in sarcoidosis patients. ERJ Open Res. 2026 Aug 17;12(4):01521-2025. doi: 10.1183/23120541.01521-2025. eCollection 2026 Jul.
PubMed 42609693
Study at a glance
From the registry record, last updated by the sponsor on 3 Mar 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Role of Monocytes (Mo) and Macrophages (Ma) in Sarcoidosis and in Tuberculosis
- ClinicalTrials.gov ID
- NCT05916638
- Acronym / sponsor ID
- MOSAR / APHP230273
- Conditions
- Sarcoidosis, Tuberculosis
- Keywords
- tuberculosis, sarcoidosis, granuloma, monocytes, macrophages
- Study type
- Observational
- Recruitment status
- Recruiting
- Enrolment
- 100 participants (estimated)
- Lead sponsor
- Assistance Publique - Hôpitaux de ParisUniversity, hospital or other
- Study start
- 15 Jan 2024 (actual)
- Primary completion
- Jan 2029 (estimated)
- Study completion
- Jan 2030 (estimated)
- First posted
- 23 Jun 2023 (actual)
- 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.
Sarcoidosis is a systemic inflammatory disease characterized by unspecific granuloma formation. Our hypothesis is that granuloma formation and maintenance mainly relies on the overactivation of monocytes (Mo) and macrophages (Ma). To this end, the study aims (i) to define MoMa systemic signature in sarcoidosis, (ii) to characterize this signature in situ on tissue samples, and (iii) to identify causative factors that participate to the MoMa chronic overactivation. Thus, a cohort of sarcoidosis patients will be compared with tuberculosis patients. The MoMa systemic signature will be defined on whole blood (TruCulture model) and then in situ through different methods (multi-parameter spectral flow cytometry, RNA-seq, Luminex, imaging mass cytometry). The epigenome of monocytes will be studied thanks to CUT\&Tag. The MoMa systemic signature will be defined ex vivo at different time points during the course of the disease with phenotypic, transcriptomic, cytokine and functional approaches. The previously identified signature will be studied in situ and completed by the characterization of granuloma architecture and microenvironmental interactions, which could be modulated by epigenetic modifications. Hence, the epigenome of monocytes will be analyzed in two groups (sarcoidosis and tuberculosis). These results would allow to better understand sarcoidosis physiopathology and, in fine, may raise new therapeutic strategies. Finally, the study could challenge the dogma on innate immunity/auto-inflammation versus adaptive immunity/auto-immunity/memory.
Detailed description
"Sarcoidosis is an inflammatory disease characterized by the presence of coalescing, tightly clustered, non-necrotizing granulomas. The diagnosis is based on three major criteria: a compatible clinical presentation, the presence of non-necrotizing granulomatous inflammation, and the exclusion of alternative granulomatous diseases. A wide range of clinical phenotypes are observed depending on the location of the granulomatous lesions which can affect any organ, with the lungs being the most affected site. Sarcoidosis shares many similarities with tuberculosis, in which granuloma formation is triggered by Mycobacterium tuberculosis (M. tb). These phenotypic similarities between the two diseases present many challenges for diagnosis, clinical management and therapy.
Our understanding of the factors that contribute to sarcoidosis development, granuloma formation and maintenance remains limited. Part of this challenge is that granuloma development may involve both environmental and genetic factors, which contribute to the recruitment of immune cells to form the granuloma. Immune cells involved in the granuloma include (1) CD4 Th1 and Th17 T cells and their associated cytokines (e.g, IFNγ, TNFα, IL-17, IL-2); and (2) monocytes (Mo) and macrophages (Ma) including proinflammatory M1 and pro-fibrosis M2 types. However, the specific factors that contribute to granuloma maintenance and evolution remain to be identified. Among them, we can hypothesized that trained immunity, persistence of the antigen, or the microenvironment are involved in this chronic dysregulated immune response. Such an improved understanding of the pathophysiology of the disease may allow development of new treatments, as currently corticosteroids remain the mainstay of therapy.
Our main hypothesis is that granuloma formation and maintenance mainly relies on the overactivation of monocytes (Mo) and macrophages (Ma). To this end, the study aims (i) to define MoMa systemic signature in sarcoidosis, (ii) to characterize this signature in situ on tissue samples, and (iii) to identify causative factors that participate to the MoMa chronic overactivation. Thus, a cohort of sarcoidosis patients will be compared with tuberculosis patients. The MoMa systemic signature will be defined on whole blood (TruCulture model) and then in situ through different methods (multi-parameter spectral flow cytometry, RNA-seq, Luminex, imaging mass cytometry). The epigenome of monocytes will be studied thanks to CUT\&Tag. The MoMa systemic signature will be defined ex vivo at different time points (M0, M6 and M12) during the course of the disease with phenotypic, transcriptomic, cytokine and functional approaches. The previously identified signature will be studied in situ and completed by the characterization of granuloma architecture and microenvironmental interactions, which could be modulated by epigenetic modifications. Hence, the epigenome of monocytes will be analyzed in two groups (sarcoidosis and tuberculosis). These results would allow to better understand sarcoidosis physiopathology and, in fine, may raise new therapeutic strategies. Finally, the study could challenge the dogma on innate immunity/auto-inflammation versus adaptive immunity/auto-immunity/memory."
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Sarcoidosis | – | Other: blood samplepatients diagnosed with sarcoidosis |
| Tuberculosis | – | Other: blood samplepatients diagnosed with tuberculosis |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Adult patients diagnosed with sarcoidosis or tuberculosis
Key inclusion criteria (3 listed)
- Male and female > 18 years old
- Diagnosis of sarcoidosis and of tuberculosis
- Affiliated to medical insurance
Key exclusion criteria (4 listed)
- HIV infection
- pregnant or breastfeeding woman
- Patient under legal protection, guardianship or curators
- Absence of signed consent" Secondary exclusion criteria Other causes of granulomatosis ultimately identified as sarcoidosis or tuberculosis
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| blood sampleblood sample collection | Other | Sarcoidosis, Tuberculosis |
Primary outcome
macrophage activation in sarcoidosis measured by epigenomic
Time frame: up to 12 months of follow-up.
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
monocyte activation in sarcoidosis measured by epigenomic
Time frame: up to 12 months of follow-up.
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
macrophage activation in sarcoidosis measured by spatial transcriptomics
Time frame: up to 12 months of follow-up.
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
monocyte activation in sarcoidosis measured by spatial transcriptomics
Time frame: up to 12 months of follow-up.
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
monocyte activation in sarcoidosis measured by transcriptomic
Time frame: up to 12 months of follow-up.
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
macrophage activation in sarcoidosis measured by transcriptomic
Time frame: up to 12 months of follow-up.
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
macrophage activation in sarcoidosis measured by cytokine measurement
Time frame: up to 12 months of follow-up.
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
monocyte activation in sarcoidosis measured by cytokine measurement
Time frame: up to 12 months of follow-up.
performed on peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood
6 secondary outcomes
monocyte activation in tuberculosis measured by epigenomic
Time frame: up to 12 months of follow-up.
Identification of a pathogen that triggers sarcoidosis development by metagenomic study
Time frame: Samples collected before treatment/at diagnosis
identification of epigenetic modifications of monocytes by CUT&Tag method
Time frame: 12 months of follow-up.
Identification of a diagnostic test to discriminate sarcoidosis and tuberculosis
Time frame: Samples collected before treatment/at diagnosis
real-time analysis of oxidative phosphorylation of monocyte
Time frame: up to 12 months of follow-up
real-time analysis of glycolysis of monocytes
Time frame: up to 12 month of follow up
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 Mar 2026.
- Derived from this study: PubMed 42609693Robert M, Boizeau L, Cappy P, Villain E, Culina S, Sannier A, Yatim N, Mageau A, Charles N, Rodriguez C, Peiffer-Smadja N, Borie R, Duffy D, Woerther PL, Sacre K. Systemic and local lymph node inflammation at disease onset in sarcoidosis patients. ERJ Open Res. 2026 Aug 17;12(4):01521-2025. doi: 10.1183/23120541.01521-2025. eCollection 2026 Jul.
- Individual participant dataSharing planned: Undecided
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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.
Karim SACRE, MD-PhD, PU-PH principal investigator
Assistance Publique - Hôpitaux de Paris
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 Sarcoidosis and Tuberculosis, run by Assistance Publique - Hôpitaux de Paris at 1 site in France.
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 3 inclusion and 4 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: looking for participants now, as of the sponsor's last update on 3 Mar 2026. 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 France. 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?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Karim Sacre, MD-PhD, PU-PH (0140256019 ext. +33, karim.sacre@aphp.fr), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
macrophage activation in sarcoidosis measured by epigenomic (time frame: up to 12 months of follow-up.). The study lists 8 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05916638, which also lists 1 linked publication.
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 3 Mar 2026.