"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

***********

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]

Well worth keeping an eye on.  Will be looking forward to more research on this, and a wider study.

Thanks, Jim, for pointing this out.

Best wishes,

George

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


Quote:

methylprednisolone acetate - The acetate salt of a synthetic glucocorticoid receptor agonist with immunosuppressive and antiinflammatory effects. Methylprednisolone acetate is converted into active prednisolone in the body, which activates glucocorticoid receptor mediated gene expression. This includes inducing synthesis of anti-inflammatory protein IkappaB-alpha and inhibiting synthesis of nuclear factor kappaB (NF-kappaB). As a result, proinflammatory cytokine production such as IL-1, IL-2 and IL-6 is down-regulated and cytotoxic T-lymphocyte activation is inhibited. Therefore, an overall reduction in chronic inflammation and autoimmune reactions may be achieved.

source
START PRINTPAGEMultimedia File Viewing and Clickable Links are available for Registered Members only!!  You need to or END PRINTPAGE