Congratulations Dr. Deepa Avadhani and the entire Sri Ramachandra team (Nisha Smithi, Pooja Singh, Swathika Rajendran, Harini Purushothaman, Ameena Bee, Vishnupriya Gurumoorthy Mani, Sowmiya Mari, Rajesh Kumar Gandhirajan, Murugesan Arumugam. WHS President Prof Lakshmi Narasimhan on this important publication in Journal of Neuroimmunology (online Nov 30, 2025; 2026 issue) !
― Dr. Pravin Thomas
What the paper shows:
They studied B-cell immune signaling across migraine phases (pre-ictal → ictal → post-ictal) vs healthy controls.
BAFF (TNFSF13B) was consistently higher in migraine, with a clear peak during the ictal phase (p=0.011), then falling post-ictally.
APRIL (TNFSF13) was downregulated across phases (trend)
Message: a divergent BAFF↑ / APRIL↓ “B-cell immune signature” that tracks with the attack state.
Why this may be path-breaking (and how it compares globally):
Worldwide, most “immune migraine” biomarker work has largely focused on cytokines (IL-6, TNF-α, IL-1β, etc.), with mixed/variable ictal vs interictal results and major sampling variability.
This study is novel because it moves upstream to TNF-superfamily B-cell regulators (BAFF/APRIL) and maps them across migraine phases, suggesting a more structured immune pathway signal rather than just “noisy cytokine snapshots.”
What it could eventually enable:
A phase-sensitive blood biomarker panel (attack biology, stratification, maybe even risk prediction in future studies).
A stronger mechanistic bridge between migraine and autoimmune-like immune dysregulation (consistent with broader scoping work on altered immunity in migraine). A possible long-term therapeutic conversation around BAFF/APRIL pathway modulation, given that BAFF/APRIL antagonism is already a serious drug-development space in autoimmunity. We need larger studies though, looking for correlation with disability/phenotype/treatment response yet).
A genuinely exciting “first signal” that migraine biology may include a distinct B-cell immune axis with BAFF peaking during attacks and APRIL suppression, potentially more mechanistically informative than many prior cytokine-only studies. With validation in larger cohorts + protein assays + phenotype correlations, this line of work has real potential to influence how we classify and biologically stratify migraine in the future.
Those who wish to do further studies in this direction can contact Dr. Deepa Avadhani DM, FIHN, WHS Fellow
