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Research Article Free access | 10.1172/JCI119850

Preferential localization of systemically administered radiolabeled interleukin 1alpha in experimental inflammation in mice by binding to the type II receptor.

C J van der Laken, O C Boerman, W J Oyen, M T van de Ven, R Chizzonite, F H Corstens, and J W van der Meer

Department of Nuclear Medicine, University Hospital Nijmegen, 6500 HB Nijmegen, The Netherlands. J.vanderLaken@Nugen.AZN.NL

Find articles by van der Laken, C. in: PubMed | Google Scholar

Department of Nuclear Medicine, University Hospital Nijmegen, 6500 HB Nijmegen, The Netherlands. J.vanderLaken@Nugen.AZN.NL

Find articles by Boerman, O. in: PubMed | Google Scholar

Department of Nuclear Medicine, University Hospital Nijmegen, 6500 HB Nijmegen, The Netherlands. J.vanderLaken@Nugen.AZN.NL

Find articles by Oyen, W. in: PubMed | Google Scholar

Department of Nuclear Medicine, University Hospital Nijmegen, 6500 HB Nijmegen, The Netherlands. J.vanderLaken@Nugen.AZN.NL

Find articles by van de Ven, M. in: PubMed | Google Scholar

Department of Nuclear Medicine, University Hospital Nijmegen, 6500 HB Nijmegen, The Netherlands. J.vanderLaken@Nugen.AZN.NL

Find articles by Chizzonite, R. in: PubMed | Google Scholar

Department of Nuclear Medicine, University Hospital Nijmegen, 6500 HB Nijmegen, The Netherlands. J.vanderLaken@Nugen.AZN.NL

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Department of Nuclear Medicine, University Hospital Nijmegen, 6500 HB Nijmegen, The Netherlands. J.vanderLaken@Nugen.AZN.NL

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Published December 15, 1997 - More info

Published in Volume 100, Issue 12 on December 15, 1997
J Clin Invest. 1997;100(12):2970–2976. https://doi.org/10.1172/JCI119850.
© 1997 The American Society for Clinical Investigation
Published December 15, 1997 - Version history
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Abstract

Previously, we have shown that systemically administered radiolabeled interleukin 1alpha (IL-1alpha) accumulates preferentially in inflammatory foci in mice. Since inflammation is characterized by influx of leukocytes, which represent IL-1 receptor (IL-1R) positive cells, radiolabeled IL-1 may specifically localize in inflammation by binding to its receptors on infiltrated leukocytes. This hypothesis was tested in a series of studies in mice with acute focal inflammations. Evidence for specific IL-1-IL-1R interaction in induced inflammation was found: microscopic autoradiography revealed that 125I-IL-1alpha localized at the site of inflammatory cells with time; 125I-myoglobin, a similar-sized protein with no known interactions in vivo, was not retained in the inflammation. Furthermore, the uptake 125I-IL-1alpha in inflammatory tissue was significantly lower in neutropenic mice than in immunocompetent mice (0.05+/-0.004 vs. 0.65+/-0.06% ID/g at 48 h after injection, P < 0.0007). Moreover, the uptake of 125I-IL-1alpha at the inflammatory site could be blocked with the anti-IL-1R type II antibody 4E2. At 48 h after injection, the uptake with and without blocking the type II IL-1R was 0.13+/-0.01 and 0. 65+/-0.05% ID/g, respectively (P < 0.0001). These in vivo studies provide evidence that systemically administered radiolabeled IL-1alpha localizes in inflammatory tissue by specific receptor binding, predominantly by binding to the type II IL-1R.

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