Chronic MigraineSIIM-regNCT07067112
Suppressive Functions of Regulatory T Cells in Migraine
A study testing Blood sampling, questionnaire and phone call in people with Chronic Migraine, run by University Hospital, Clermont-Ferrand at 1 site in France.
Trial summary
Migraine is a frequent, disabling condition, of great social and economical impact worldwide. This condition is more frequent in women and subjects with autoimmune and/or inflammatory diseases. Cytokine and immune cell dysregulations have been evidenced in migraine. Read more about this study
- Who is it for?
- Ages 18 to 50 years, women onlyHealthy volunteers can take part
- Conditions the study is for
- Chronic Migraine
- What is being tested?
- Blood sampling, questionnaire and phone call
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 24 participants
- Where
- 1 siteFrance
- Study dates
- 10 Sep 2026to 30 Nov 2027
- Phase
- Interventional
- 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 to 50 years
- Women only
- Healthy volunteers accepted
- Adult
Who may be able to join
- Females
- 18 to 50 years old
- For chronic migrain : At least 8 monthly migraine days
Who cannot join
- BMI < or = 17kg/m² or > or = 30kg/m²
- Diagnosis or suspicion of type 2 diabetes, auto-immune or inflammatory diseases, immunodeficiency diseases
- Diagnosis of headache of non-migraine origin, except for tension type headache (i.e.: cluster headache, post-traumatic headache, cerebral tumour…)
- For controls participants : tension type headache with 4 or more monthly headache days
- Pregnancy, delivery, miscarriage, breastfeeding, participation in a medically assisted human reproduction program (ovary stimulation/hormone therapy) < 3 months before blood sampling
- Menopause, hysterectomy, or bilateral oophorectomy
Show all 13Show fewer
- Modification of prophylactic anti-migraine therapy (start, change of molecule, interruption) < 1 month before blood sampling (for migraine participants)
- Hormone therapy (beside contraception and treatment of endometriosis)
- Transplantation (solid organ or bone marrow)
- Cancer (active or remitting) < 1 year before blood sampling (solid organ or blood)
- Haematologic disease (benign or malignant) of the lymphoid lineage
- Guardianship, curatorship, safeguard of justice or deprivation of liberty
- For controls : history of migraine
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
CHU Clermont-Ferrand
Clermont-Ferrand
Lise LACLAUTRE, 0473754963, llaclautre_perrier@chu-clermontferrand.fr
Xavier MOISSET
About this study
Migraine is a frequent, disabling condition, of great social and economical impact worldwide. This condition is more frequent in women and subjects with autoimmune and/or inflammatory diseases. Cytokine and immune cell dysregulations have been evidenced in migraine. Inflammation seems to play an important role in migraine chronification; however, the inflammatory mechanisms involved in migraine pathophysiology remain unclear. Regulatory T (Treg) cells play a central role in maintaining immune homeostasis. They regulate effector T (Teff) cell proliferation and cytokine production, through several suppressive mechanisms, such as the hydrolysis of adenosine triphosphate (ATP) into adenosine (ADO), mediated by surface enzymes Cluster Differentiation 39 (CD39) and Cluster Differentiation 73 (CD73). ATP is involved in pain processes in migraine, and insufficient hydrolysis could participate in pain chronification. Recent studies suggest altered proportions of Treg cells in migraine, and decreased levels of CD39-positive (CD39+) Treg cells, suggesting Treg suppressive functions may be decreased in the disease. However, there have been no functional studies to date to confirm this hypothesis.
The investigators believe Treg suppressive functions may be decreased in migraine, and that such alterations may be caused by a malfunction in the ADO pathway.
Read the detailed description
Migraine is a major and global public health concern that affects 14% of the population worldwide. It is 2 to 3 times more prevalent in women than men and is the second leading cause of disability. Many patients remain unresponsive to currently available treatments. As evidenced in different studies, including our own, several auto-immune and inflammatory disorders, such as multiple sclerosis, are associated with a higher prevalence of migraine and a higher risk for migraine chronification (at least 15 headache days per month) compared to the general population. These findings suggest that inflammation may play an important role in migraine chronification. Cytokine and immune cell dysregulations have been evidenced in the disease but the role of inflammation in migraine pathophysiology remains unclear. Among T lymphocytes, regulatory T (Treg) cells play an important role in maintaining immune homeostasis. They regulate pro-inflammatory effector T (Teff) cells and proinflammatory cytokine release (IL-6, IL-17, interferon-γ) through different suppressive mechanisms such as the hydrolysis of pro-inflammatory and nociceptive adenosine triphosphate (ATP) into anti-inflammatory and antinociceptive adenosine (ADO), by Treg surface enzymes CD39 and CD73, present on 40% and 6-10% of Treg cells, respectively. ADO then suppresses Teff cells by binding to their ADO receptor A2A. ATP is involved in the transduction of pain signals in migraine and its insufficient hydrolysis can lead to pain chronification. It has been evidenced that Tregs naturally suppress interferon (IFN)-γ production by Teff cells. Their CD39-positive (CD39+) subsets also suppress IL-17 production by Teff cells, whereas CD39-negative (CD39-) Tregs seem to increase IL-17 secretion. Recent studies have shown altered Treg proportions in migraine compared to controls and Treg subpopulation dysregulations, such as decreased CD39+Treg cell levels. This further suggests that Treg suppressive functions may be altered in migraine, but no functional assays have been led to confirm that.
In this study, the investigators aim to determine whether Treg cells play a role in migraine pathophysiology, by answering the following 3 separate questions: Question 1) Are Treg suppressive functions decreased in migraine patients? Question 2) Are CD39+Treg cells functionally deficient in migraine patients? Question 3) Is the hydrolytic activity of enzyme CD39 reduced in migraine patients?
Through Treg/Teff coculture the investigators will assess the ability of total Treg and CD39+Treg cells to inhibit Teff proliferation and pro-inflammatory cytokine secretion and measure the hydrolytic activity of Treg enzyme CD39 on ATP in chronic migraine patients versus healthy controls. The use of human immune cells (Treg and Teff lymphocytes) in our experiments will allow the investigators to better understand migraine pathophysiology, with a direct application to human subjects, as well as to avoid animal testing and suffering. Through its animal-free setting, following the 'Reduce, Refine, Replace (3Rs)' principle, the investigators wish to promote animal-free research and the reduction of animal use for reagent production by using recombinant antibodies for flow cytometry and synthetic medium supplements for cell culture. This study will lead to a better understanding of the role of inflammation and Treg cells in migraine pathophysiology and will provide new perspectives for the development of personalized treatments according to the immune pain profile of migraine patients.
The investigators aim to show that Treg suppressive functions are altered in migraine and that the ADO pathway is deficient. Through Treg/Teff coculture the investigators will measure the ability of Tregs to inhibit Teff proliferation and cytokine secretion and assess the CD39-related hydrolytic activity of Tregs. This will allow the investigators to study Treg cells suppressive functions on Teff cells in female patients with chronic migraine and healthy female control participants.
- Conditions
- Chronic Migraine
- Being tested
- Blood sampling, questionnaire and phone call
- Keywords
- Migraine, Inflammation, Immune system, Regulatory T cells
- Medical subject headings
- Migraine Disorders, Inflammation
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Blood sampling, questionnaire and phone callBiological
The blood sample will drawn outside of a migraine attack (no migraine within 6 hours prior to the blood test), and the questionnaire will be auto-administered
| Study group | Role | What they receive |
|---|---|---|
| Chronic migraine | Experimental | Chronic migraine patients will donate 100 milliliters (mL) of peripheral and venous blood, answer a questionnaire and 2 phone calls (one at day 1 and the other at day 3 from the blood test). Receives: Biological: Blood sampling, questionnaire and phone call |
| Controls | Experimental | Non-migraine controls will donate 100 mL of peripheral and venous blood, answer a questionnaire and 2 phone calls (one at day 1 and the other at day 3 from the blood test). Receives: Biological: Blood sampling, questionnaire and phone call |
What is being measured
The primary outcome is the main question the study is designed to answer.
Treg cell suppressive functions
To measure the suppressive effect of Treg cells on Teff cells in chronic migraine patients and healthy controls
Measured: Day 0
Secondary outcomes (3)
CD39+ Treg cell suppressive functions
To measure the suppressive effect of CD39+Treg cells on Teff cells in chronic migraine patients and healthy controls
Measured: Day 0
CD39 activity
To measure the hydrolytic activity of Treg enzyme CD39 in chronic migraine patients and healthy controls
Measured: Day 0
Cytokines
To measure the levels of cytokine levels in blood : interleukin (IL)-6, IL-10, IL-17, IFN-g and transforming growth factor b
Measured: Day 0
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted16 Jul 2025
- Study start10 Sep 2026
- Primary completion30 Nov 2027 (estimated)
- Study completion30 Nov 2027 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (19)Papers the sponsor has linked to this study.
- Other trials for Chronic MigraineStudies of the same condition, open and under way.
- More trials run by University Hospital, Clermont-FerrandThe 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
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Model description
- Participants will be enrolled in either the chronic migraine or control group for comparison between chronic migraine patients and controls.
- Masking
- None (open label)
- Enrolment
- 24 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University Hospital, Clermont-Ferrand
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Xavier MOISSET, Principal investigator, University Hospital, Clermont-Ferrand
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07067112
- Sponsor's protocol ID
- RBHP 2025 MOISSET
- Acronym
- SIIM-reg
- Status last verified
- Oct 2026
- First submitted
- 4 Jul 2025
- Last updated
- 14 Oct 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Stovner LJ, Hagen K, Linde M, Steiner TJ. The global prevalence of headache: an update, with analysis of the influences of methodological factors on prevalence estimates. J Headache Pain. 2022 Apr 12;23(1):34. doi: 10.1186/s10194-022-01402-2.
PubMed 35410119Ashina M. Migraine. N Engl J Med. 2020 Nov 5;383(19):1866-1876. doi: 10.1056/NEJMra1915327. No abstract available.
PubMed 33211930Barbanti P, Aurilia C, Egeo G, Torelli P, Proietti S, Cevoli S, Bonassi S; Italian Migraine Registry study group. Late Response to Anti-CGRP Monoclonal Antibodies in Migraine: A Multicenter Prospective Observational Study. Neurology. 2023 Sep 12;101(11):482-488. doi: 10.1212/WNL.0000000000207292. Epub 2023 Apr 18.
PubMed 37072224Moisset X, Giraud P, Dallel R. Migraine in multiple sclerosis and other chronic inflammatory diseases. Rev Neurol (Paris). 2021 Sep;177(7):816-820. doi: 10.1016/j.neurol.2021.07.005. Epub 2021 Jul 27.
PubMed 34325914Moisset X, Ouchchane L, Guy N, Bayle DJ, Dallel R, Clavelou P. Migraine headaches and pain with neuropathic characteristics: comorbid conditions in patients with multiple sclerosis. Pain. 2013 Dec;154(12):2691-2699. doi: 10.1016/j.pain.2013.07.050. Epub 2013 Aug 2.
PubMed 23911697Edvinsson L, Haanes KA, Warfvinge K. Does inflammation have a role in migraine? Nat Rev Neurol. 2019 Aug;15(8):483-490. doi: 10.1038/s41582-019-0216-y. Epub 2019 Jul 1.
PubMed 31263254Thuraiaiyah J, Erritzoe-Jervild M, Al-Khazali HM, Schytz HW, Younis S. The role of cytokines in migraine: A systematic review. Cephalalgia. 2022 Dec;42(14):1565-1588. doi: 10.1177/03331024221118924. Epub 2022 Aug 12.
PubMed 35962530Nurkhametova D, Kudryavtsev I, Khayrutdinova O, Serebryakova M, Altunbaev R, Malm T, Giniatullin R. Purinergic Profiling of Regulatory T-cells in Patients With Episodic Migraine. Front Cell Neurosci. 2018 Sep 25;12:326. doi: 10.3389/fncel.2018.00326. eCollection 2018.
PubMed 30319363Loza MJ, Anderson AS, O'Rourke KS, Wood J, Khan IU. T-cell specific defect in expression of the NTPDase CD39 as a biomarker for lupus. Cell Immunol. 2011;271(1):110-7. doi: 10.1016/j.cellimm.2011.06.010. Epub 2011 Jul 18.
PubMed 21763644Vignali DA, Collison LW, Workman CJ. How regulatory T cells work. Nat Rev Immunol. 2008 Jul;8(7):523-32. doi: 10.1038/nri2343.
PubMed 18566595Giniatullin R, Nistri A, Fabbretti E. Molecular mechanisms of sensitization of pain-transducing P2X3 receptors by the migraine mediators CGRP and NGF. Mol Neurobiol. 2008 Feb;37(1):83-90. doi: 10.1007/s12035-008-8020-5. Epub 2008 May 6.
PubMed 18459072Fletcher JM, Lonergan R, Costelloe L, Kinsella K, Moran B, O'Farrelly C, Tubridy N, Mills KH. CD39+Foxp3+ regulatory T Cells suppress pathogenic Th17 cells and are impaired in multiple sclerosis. J Immunol. 2009 Dec 1;183(11):7602-10. doi: 10.4049/jimmunol.0901881. Epub 2009 Nov 16.
PubMed 19917691Faraji F, Shojapour M, Farahani I, Ganji A, Mosayebi G. Reduced regulatory T lymphocytes in migraine patients. Neurol Res. 2021 Aug;43(8):677-682. doi: 10.1080/01616412.2021.1915077. Epub 2021 Apr 14.
PubMed 33853506Arumugam M, Parthasarathy V. Reduction of CD4(+)CD25(+) regulatory T-cells in migraine: Is migraine an autoimmune disorder? J Neuroimmunol. 2016 Jan 15;290:54-9. doi: 10.1016/j.jneuroim.2015.11.015. Epub 2015 Nov 28.
PubMed 26711570Yang L, Zhou Y, Zhang L, Wang Y, Zhang Y, Xiao Z. Aryl hydrocarbon receptors improve migraine-like pain behaviors in rats through the regulation of regulatory T cell/T-helper 17 cell-related homeostasis. Headache. 2023 Sep;63(8):1045-1060. doi: 10.1111/head.14599. Epub 2023 Aug 4.
PubMed 37539825
Study at a glance
From the registry record, last updated by the sponsor on 14 Oct 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Suppressive Functions of Regulatory T Cells in Migraine
- ClinicalTrials.gov ID
- NCT07067112
- Acronym / sponsor ID
- SIIM-reg / RBHP 2025 MOISSET
- Conditions
- Chronic Migraine
- Keywords
- Migraine, Inflammation, Immune system, Regulatory T cells
- Study type
- Interventional
- Recruitment status
- Recruiting
- Enrolment
- 24 participants (estimated)
- Lead sponsor
- University Hospital, Clermont-FerrandUniversity, hospital or other
- Study start
- 10 Sep 2026 (actual)
- Primary completion
- 30 Nov 2027 (estimated)
- Study completion
- 30 Nov 2027 (estimated)
- First posted
- 16 Jul 2025 (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.
Migraine is a frequent, disabling condition, of great social and economical impact worldwide. This condition is more frequent in women and subjects with autoimmune and/or inflammatory diseases. Cytokine and immune cell dysregulations have been evidenced in migraine. Inflammation seems to play an important role in migraine chronification; however, the inflammatory mechanisms involved in migraine pathophysiology remain unclear. Regulatory T (Treg) cells play a central role in maintaining immune homeostasis. They regulate effector T (Teff) cell proliferation and cytokine production, through several suppressive mechanisms, such as the hydrolysis of adenosine triphosphate (ATP) into adenosine (ADO), mediated by surface enzymes Cluster Differentiation 39 (CD39) and Cluster Differentiation 73 (CD73). ATP is involved in pain processes in migraine, and insufficient hydrolysis could participate in pain chronification. Recent studies suggest altered proportions of Treg cells in migraine, and decreased levels of CD39-positive (CD39+) Treg cells, suggesting Treg suppressive functions may be decreased in the disease. However, there have been no functional studies to date to confirm this hypothesis.
The investigators believe Treg suppressive functions may be decreased in migraine, and that such alterations may be caused by a malfunction in the ADO pathway.
Detailed description
Migraine is a major and global public health concern that affects 14% of the population worldwide. It is 2 to 3 times more prevalent in women than men and is the second leading cause of disability. Many patients remain unresponsive to currently available treatments. As evidenced in different studies, including our own, several auto-immune and inflammatory disorders, such as multiple sclerosis, are associated with a higher prevalence of migraine and a higher risk for migraine chronification (at least 15 headache days per month) compared to the general population. These findings suggest that inflammation may play an important role in migraine chronification. Cytokine and immune cell dysregulations have been evidenced in the disease but the role of inflammation in migraine pathophysiology remains unclear. Among T lymphocytes, regulatory T (Treg) cells play an important role in maintaining immune homeostasis. They regulate pro-inflammatory effector T (Teff) cells and proinflammatory cytokine release (IL-6, IL-17, interferon-γ) through different suppressive mechanisms such as the hydrolysis of pro-inflammatory and nociceptive adenosine triphosphate (ATP) into anti-inflammatory and antinociceptive adenosine (ADO), by Treg surface enzymes CD39 and CD73, present on 40% and 6-10% of Treg cells, respectively. ADO then suppresses Teff cells by binding to their ADO receptor A2A. ATP is involved in the transduction of pain signals in migraine and its insufficient hydrolysis can lead to pain chronification. It has been evidenced that Tregs naturally suppress interferon (IFN)-γ production by Teff cells. Their CD39-positive (CD39+) subsets also suppress IL-17 production by Teff cells, whereas CD39-negative (CD39-) Tregs seem to increase IL-17 secretion. Recent studies have shown altered Treg proportions in migraine compared to controls and Treg subpopulation dysregulations, such as decreased CD39+Treg cell levels. This further suggests that Treg suppressive functions may be altered in migraine, but no functional assays have been led to confirm that.
In this study, the investigators aim to determine whether Treg cells play a role in migraine pathophysiology, by answering the following 3 separate questions: Question 1) Are Treg suppressive functions decreased in migraine patients? Question 2) Are CD39+Treg cells functionally deficient in migraine patients? Question 3) Is the hydrolytic activity of enzyme CD39 reduced in migraine patients?
Through Treg/Teff coculture the investigators will assess the ability of total Treg and CD39+Treg cells to inhibit Teff proliferation and pro-inflammatory cytokine secretion and measure the hydrolytic activity of Treg enzyme CD39 on ATP in chronic migraine patients versus healthy controls. The use of human immune cells (Treg and Teff lymphocytes) in our experiments will allow the investigators to better understand migraine pathophysiology, with a direct application to human subjects, as well as to avoid animal testing and suffering. Through its animal-free setting, following the 'Reduce, Refine, Replace (3Rs)' principle, the investigators wish to promote animal-free research and the reduction of animal use for reagent production by using recombinant antibodies for flow cytometry and synthetic medium supplements for cell culture. This study will lead to a better understanding of the role of inflammation and Treg cells in migraine pathophysiology and will provide new perspectives for the development of personalized treatments according to the immune pain profile of migraine patients.
The investigators aim to show that Treg suppressive functions are altered in migraine and that the ADO pathway is deficient. Through Treg/Teff coculture the investigators will measure the ability of Tregs to inhibit Teff proliferation and cytokine secretion and assess the CD39-related hydrolytic activity of Tregs. This will allow the investigators to study Treg cells suppressive functions on Teff cells in female patients with chronic migraine and healthy female control participants.
Study design
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 2
- Model description
- Participants will be enrolled in either the chronic migraine or control group for comparison between chronic migraine patients and controls.
| Arm | Type | Receives |
|---|---|---|
| Chronic migraine | Experimental | Biological: Blood sampling, questionnaire and phone callChronic migraine patients will donate 100 milliliters (mL) of peripheral and venous blood, answer a questionnaire and 2 phone calls (one at day 1 and the other at day 3 from the blood test). |
| Controls | Experimental | Biological: Blood sampling, questionnaire and phone callNon-migraine controls will donate 100 mL of peripheral and venous blood, answer a questionnaire and 2 phone calls (one at day 1 and the other at day 3 from the blood test). |
Who may qualify
- Ages
- 18 to 50 years
- Sex
- Female only
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (3 listed)
- Females
- 18 to 50 years old
- For chronic migrain : At least 8 monthly migraine days
Key exclusion criteria (13 listed)
- BMI < or = 17kg/m² or > or = 30kg/m²
- Diagnosis or suspicion of type 2 diabetes, auto-immune or inflammatory diseases, immunodeficiency diseases
- Diagnosis of headache of non-migraine origin, except for tension type headache (i.e.: cluster headache, post-traumatic headache, cerebral tumour…)
- For controls participants : tension type headache with 4 or more monthly headache days
- Pregnancy, delivery, miscarriage, breastfeeding, participation in a medically assisted human reproduction program (ovary stimulation/hormone therapy) < 3 months before blood sampling
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 sampling, questionnaire and phone callThe blood sample will drawn outside of a migraine attack (no migraine within 6 hours prior to the blood test), and the questionnaire will be auto-administered | Biological | Chronic migraine, Controls |
Primary outcome
Treg cell suppressive functions
Time frame: Day 0
To measure the suppressive effect of Treg cells on Teff cells in chronic migraine patients and healthy controls
3 secondary outcomes
CD39+ Treg cell suppressive functions
Time frame: Day 0
CD39 activity
Time frame: Day 0
Cytokines
Time frame: Day 0
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 14 Oct 2026.
- Background: PubMed 35410119Stovner LJ, Hagen K, Linde M, Steiner TJ. The global prevalence of headache: an update, with analysis of the influences of methodological factors on prevalence estimates. J Headache Pain. 2022 Apr 12;23(1):34. doi: 10.1186/s10194-022-01402-2.
- Background: PubMed 33211930Ashina M. Migraine. N Engl J Med. 2020 Nov 5;383(19):1866-1876. doi: 10.1056/NEJMra1915327. No abstract available.
- Background: PubMed 37072224Barbanti P, Aurilia C, Egeo G, Torelli P, Proietti S, Cevoli S, Bonassi S; Italian Migraine Registry study group. Late Response to Anti-CGRP Monoclonal Antibodies in Migraine: A Multicenter Prospective Observational Study. Neurology. 2023 Sep 12;101(11):482-488. doi: 10.1212/WNL.0000000000207292. Epub 2023 Apr 18.
- Background: PubMed 34325914Moisset X, Giraud P, Dallel R. Migraine in multiple sclerosis and other chronic inflammatory diseases. Rev Neurol (Paris). 2021 Sep;177(7):816-820. doi: 10.1016/j.neurol.2021.07.005. Epub 2021 Jul 27.
- Background: PubMed 23911697Moisset X, Ouchchane L, Guy N, Bayle DJ, Dallel R, Clavelou P. Migraine headaches and pain with neuropathic characteristics: comorbid conditions in patients with multiple sclerosis. Pain. 2013 Dec;154(12):2691-2699. doi: 10.1016/j.pain.2013.07.050. Epub 2013 Aug 2.
- Background: PubMed 31263254Edvinsson L, Haanes KA, Warfvinge K. Does inflammation have a role in migraine? Nat Rev Neurol. 2019 Aug;15(8):483-490. doi: 10.1038/s41582-019-0216-y. Epub 2019 Jul 1.
- Background: PubMed 35962530Thuraiaiyah J, Erritzoe-Jervild M, Al-Khazali HM, Schytz HW, Younis S. The role of cytokines in migraine: A systematic review. Cephalalgia. 2022 Dec;42(14):1565-1588. doi: 10.1177/03331024221118924. Epub 2022 Aug 12.
- Background: PubMed 30319363Nurkhametova D, Kudryavtsev I, Khayrutdinova O, Serebryakova M, Altunbaev R, Malm T, Giniatullin R. Purinergic Profiling of Regulatory T-cells in Patients With Episodic Migraine. Front Cell Neurosci. 2018 Sep 25;12:326. doi: 10.3389/fncel.2018.00326. eCollection 2018.
- Background: PubMed 21763644Loza MJ, Anderson AS, O'Rourke KS, Wood J, Khan IU. T-cell specific defect in expression of the NTPDase CD39 as a biomarker for lupus. Cell Immunol. 2011;271(1):110-7. doi: 10.1016/j.cellimm.2011.06.010. Epub 2011 Jul 18.
- Background: PubMed 18566595Vignali DA, Collison LW, Workman CJ. How regulatory T cells work. Nat Rev Immunol. 2008 Jul;8(7):523-32. doi: 10.1038/nri2343.
- Background: PubMed 18459072Giniatullin R, Nistri A, Fabbretti E. Molecular mechanisms of sensitization of pain-transducing P2X3 receptors by the migraine mediators CGRP and NGF. Mol Neurobiol. 2008 Feb;37(1):83-90. doi: 10.1007/s12035-008-8020-5. Epub 2008 May 6.
- Background: PubMed 19917691Fletcher JM, Lonergan R, Costelloe L, Kinsella K, Moran B, O'Farrelly C, Tubridy N, Mills KH. CD39+Foxp3+ regulatory T Cells suppress pathogenic Th17 cells and are impaired in multiple sclerosis. J Immunol. 2009 Dec 1;183(11):7602-10. doi: 10.4049/jimmunol.0901881. Epub 2009 Nov 16.
- Individual participant dataSharing planned: No
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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.
Xavier MOISSET principal investigator
University Hospital, Clermont-Ferrand
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Blood sampling, questionnaire and phone call in people with Chronic Migraine, run by University Hospital, Clermont-Ferrand 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 13 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 14 Oct 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 Lise Laclautre (334.73.754.963, promo_interne_drci@chu-clermontferrand.fr), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Treg cell suppressive functions (time frame: Day 0). 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 NCT07067112, which also lists 19 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 14 Oct 2026.