Regulatory T cell frequency, but not plasma IL-33 levels, represents potential immunological biomarker to predict clinical response to intravenous immunoglobulin therapy

Maddur, Mohan S and Stephen-Victor, Emmanuel and Das, Mrinmoy and Prakhar, Praveen and Sharma, Varun K and Singh, Vikas and Rabin, Magalie and Trinath, Jamma and Balaji, Kithiganahalli N and Bolgert, Francis and Vallat, Jean-Michel and Magy, Laurent and Kaveri, Srini V and Bayry, Jagadeesh (2017) Regulatory T cell frequency, but not plasma IL-33 levels, represents potential immunological biomarker to predict clinical response to intravenous immunoglobulin therapy. In: JOURNAL OF NEUROINFLAMMATION, 14 .

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Abstract

Background: Intravenous immunoglobulin (IVIG) is a polyspecific pooled immunoglobulin G preparation and one of the commonly used therapeutics for autoimmune diseases including those of neurological origin. A recent report in murine model proposed that IVIG expands regulatory T (Treg) cells via induction of interleukin 33 (IL-33). However, translational insight on these observations is lacking. Methods: Ten newly diagnosed Guillain-Barre syndrome (GBS) patients were treated with IVIG at the rate of 0.4 g/ kg for three to five consecutive days. Clinical evaluation for muscular weakness was performed by Medical Research Council (MRC) and modified Rankin scoring (MRS) system. Heparinized blood samples were collected before and 1, 2, and 4-5 weeks post-IVIG therapy. Peripheral blood mononuclear cells were stained for surface CD4 and intracellular Foxp3, IFN-., and tumor necrosis factor alpha (TNF-a) and were analyzed by flow cytometry. IL-33 and prostaglandin E2 in the plasma were measured by ELISA. Results: The fold changes in plasma IL-33 at week 1 showed no correlation with the MRC and MRS scores at weeks 1, 2, and = 4 post-IVIG therapy. Clinical recovery following IVIG therapy appears to be associated with Treg cell response. Contrary to murine study, there was no association between the fold changes in IL-33 at week 1 and Treg cell frequency at weeks 1, 2, and = 4 post-IVIG therapy. Treg cell-mediated clinical response to IVIG therapy in GBS patients was associated with reciprocal regulation of effector T cells-expressing TNF-a. Conclusion: Treg cell expansion by IVIG in patients with autoimmune diseases lack correlation with IL-33. Treg cell frequency, but not plasma IL-33 levels, represents potential immunological biomarker to predict clinical response to IVIG therapy.

Item Type:	Journal Article
Publication:	JOURNAL OF NEUROINFLAMMATION
Additional Information:	Copy right for this article belongs to the BIOMED CENTRAL LTD, 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
Department/Centre:	Division of Biological Sciences > Microbiology & Cell Biology
Date Deposited:	26 Apr 2017 07:24
Last Modified:	26 Apr 2017 07:24
URI:	http://eprints.iisc.ac.in/id/eprint/56650

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