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DOI 10.1186/s10194-024-01800-8

Медицинская библиотека · The journal of headache and pain · 2024

Altered immunity in migraine: a comprehensive scoping review.

Ha Woo-Seok, Chu Min Kyung

СтатьяScoping ReviewПеревод пока не подготовлен

Аннотация

BACKGROUND

The pathogenesis of migraine remains unclear; however, a large body of evidence supports the hypothesis that immunological mechanisms play a key role. Therefore, we aimed to review current studies on altered immunity in individuals with migraine during and outside attacks.

METHODS

We searched the PubMed database to investigate immunological changes in patients with migraine. We then added other relevant articles on altered immunity in migraine to our search.

RESULTS

Database screening identified 1,102 articles, of which 41 were selected. We added another 104 relevant articles. We found studies reporting elevated interictal levels of some proinflammatory cytokines, including IL-6 and TNF-α. Anti-inflammatory cytokines showed various findings, such as increased TGF-β and decreased IL-10. Other changes in humoral immunity included increased levels of chemokines, adhesion molecules, and matrix metalloproteinases; activation of the complement system; and increased IgM and IgA. Changes in cellular immunity included an increase in T helper cells, decreased cytotoxic T cells, decreased regulatory T cells, and an increase in a subset of natural killer cells. A significant comorbidity of autoimmune and allergic diseases with migraine was observed.

CONCLUSIONS

Our review summarizes the findings regarding altered humoral and cellular immunological findings in human migraine. We highlight the possible involvement of immunological mechanisms in the pathogenesis of migraine. However, further studies are needed to expand our knowledge of the exact role of immunological mechanisms in migraine pathogenesis.

Для цитирования: Ha Woo-Seok, Chu Min Kyung. Altered immunity in migraine: a comprehensive scoping review.. The journal of headache and pain. 2024. DOI: 10.1186/s10194-024-01800-8.

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