"Immunological mechanisms" are mentioned. IL-2 is produced by the body during an immune response. Lots of research on IL-2 for HIV and it has proven to be ineffective in that case.

The role of the immune system in the pathophysiology of CH is a pretty interesting idea.   I hope it gets more funding beyond this preliminary pilot study.

Jim

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Acta Neurol Scand. 2010 Sep 29. doi: 10.1111/j.1600-0404.2010.01434.x. [Epub ahead of print]

Interleukin-2 gene expression in different phases of episodic cluster headache - a pilot study.
Steinberg A, Sjöstrand C, Sominanda A, Fogdell-Hahn A, Nilsson Remahl AI.

Department of Clinical Neuroscience, Division of Neurology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.

Abstract
Steinberg A, Sjöstrand C, Sominanda A, Fogdell-Hahn A, Nilsson Remahl AIM. Interleukin-2 gene expression in different phases of episodic cluster headache - a pilot study.Acta Neurol Scand: DOI: 10.1111/j.1600-0404.2010.01434.x. © 2010 John Wiley & Sons A/S. Background - The pathophysiology of cluster headache (CH) is still largely unknown. Immunological mechanisms have been suggested to be of importance. Aim - This study aimed to investigate cytokine interleukin-2 (IL-2) as a possible marker of immune system involvement in the pathophysiology of CH. Methods - Eight episodic patients with CH and 16 healthy headache-free control subjects matched for age and gender were studied. Venous blood samples were drawn from the patients with CH on three occasions; during active period between headache attacks, during an attack and in remission. Venous blood samples were drawn once from each control subject. We analysed IL-2 gene expression, using quantitative real-time polymerase chain reaction. Results -  Patients with CH had significantly increased relative IL-2 gene expression levels between headache attacks during active CH period (median 9.9 IL-2 cDNA/glyceraldehyde-3-phosphate dehydrogenase cDNA; IQR 6.2-10.3) compared to during attacks (median 2.8; IQR 0.7-3.2, P = 0.012), remission (median 1.6; IQR 0.9-1.8, P = 0.017) and controls (median 0.9; IQR 0.6-1.9, P = 0.0001). Conclusion -  The increment of IL-2 found during the active CH period may support a role for this cytokine and subsequently for the immune system in the pathophysiology of CH. An expansion of this study to a broader group of cytokines and a larger patient cohort is warranted.

PMID: 20880293 [PubMed - as supplied by publisher]

interesting.
after this,on medrol(corticosteroids)information found this on its chemical information

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