Migraine is a frequent and debilitating neurologic disorder. It is more frequent in women, and more prevalent in patients with autoimmune and/or inflammatory diseases such as multiple sclerosis (MS), rheumatoid arthritis (RA), Crohn's disease (CD), systemic lupus erythematosus (SLE) and endometriosis, whereas patients with long standing type 1 diabetes mellitus (T1DM) - an autoimmune but non inflammatory disease - seem to be less affected compared to the general population. Despite new migraine prevention treatments, a large number of patients remain unresponsive to currently available anti-migraine therapy and migraine pathophysiology remains unclear. Several peptides (calcitonin gene-related peptide (CGRP), pituitary adenylate cyclase activating peptide-38 (PACAP-38), vasoactive intestinal polypeptide (VIP)) and hormones (estrogens, prolactin) and the immune system play an important role in migraine pathophysiology. Among T lymphocytes, regulatory T (Treg) cells suppress inflammation. Studies have evidenced higher levels of inflammatory molecules (cytokines) in migraine patients and have suggested decreased proportions of Treg cells in migraine, as well as in MS, RA, CD and SLE, whereas inflammation declines and Treg levels seem increased in long-standing T1DM. Inflammation, which participates in migraine pain, seems to be a common factor for migraine and these diseases. However, these studies display conflicting results and further investigation is required to better understand the mechanisms behind migraine.
In this study, the investigators will compare Treg levels, as well as identify Treg subpopulations and measure cytokine levels in migraine and migraine-free participants with and without an autoimmune/inflammatory disorder (MS, RA, CD, SLE, T1DM and endometriosis).
female
18 - 50 years of age
at least 50 kg
autoimmune/inflammatory disease groups : with a diagnosis of multiple sclerosis, systemic lupus erythematous, rheumatoid arthritis, Crohn's disease, type 1 diabetes or endometriosis
BMI < or = 17 ou > or = 30kg/m²
type 2 diabetes, immune deficit, other chronic autoimmune or inflammatory disease
non-migraine headache, except for tension type headache of less than 4 days/month
pregnancy, delivery, miscarriage, breast-feeding, participation in a medically assisted human reproduction program (ovary stimulation/hormone therapy) < 3 months before blood sampling
Parallel
Blood test
Biological/Vaccine1 blood test of maximum 40 millilitres per patient
Treg cell levels in cell/microliter (cell/µL) and percentage (%) of white blood cells
To measure Treg cell levels in migraine and migraine-free participants, with and without autoimmune/inflammatory diseases (MS, RA, CD, SLE, endometriosis, T1DM) using flow cytometry
Cytokine levels in picogram per milliliter (pg/mL)
To measure cytokine levels (interleukin 1a and b, interleukin 2, interleukin 6, interleukin 10, interleukin 12, interleukin 17, interleukin 18, interleukin 21, interleukin 22, interleukin 23, interleukin 33, interleukin 35, interleukin 36b, interleukin 37, interleukin 38, tumor necrosis factor a, interferon g, transforming growth factor b, interleukin 1ra, C-C motif ligand 20) using a LUMINEX method
Impact of hormones (progesterone, estrogen, testosterone, follicle stimulating hormone (FSH), luteinizing hormone (LH), insulin and prolactin) levels on levels of Treg cells
To determine the impact of hormones on Treg cell levels
Impact of hormones (progesterone, estrogen, testosterone, follicle stimulating hormone (FSH), luteinizing hormone (LH), insulin and prolactin) levels on levels of cytokines
To determine the impact of hormones on cytokine levels
Impact of neuropeptides (calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), pituitary adenylate cyclase-activating polypeptide (PACAP) on Treg cell levels
To determine the impact of neuropeptides on Treg cell levels
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