The inflammatory potential of IL-2: local induction of a specific chronic granulomatous lesion in mice.

Abstract:

:Subcutaneous injection of recombinant human interleukin-2 (rhuIL-2) at 10(2)-10(4) U/mouse induced delayed (48 h) accumulation of mononuclear leukocytes with diffuse granulocytes, including eosinophils. Subcutaneous local infusion of rhuIL-2 or recombinant murine IL-2 (10(2)-10(4) U/mouse) via implanted Alzet miniosmotic pumps in mice induced chronic inflammatory lesions characterized by infiltration of large vacuolated mononuclear leukocytes, lymphoid cells, and eosinophil foci; neovascularization, with high endothelial-like cells, was prominent, exhibiting intravascular trapping and migration of large mononuclear leukocytes. Leukocyte infiltrates comprised T lymphocytes (CD4+; CD8+), B lymphocytes, and macrophages. Control infusions of bovine serum albumin (BSA) induced weak fibrotic lesions with sparse macrophage infiltration and minimal accumulation of lymphocytes; VLA4+ and ICAM-1+ leukocyte infiltrates were significantly greater in IL-2-induced lesions compared with BSA-induced lesions. Quantitative image analysis showed significantly increased lesion size in the IL-2-induced lesions compared with those induced by BSA infusion. The vascularity of IL-2-induced lesions assessed by immunostaining for platelet-endothelial cell adhesion molecule was increased compared with control, BSA-induced lesions mainly due to neovascularization. ICAM-1 and VCAM-1 expression was significantly enhanced in IL-2 lesions. No systemic pathological changes were observed following IL-2 infusion. We conclude that local slow-release of IL-2 causes the evolution and maintenance of a specific chronic inflammatory lesion.

journal_name

J Leukoc Biol

authors

Dunn CJ,Hardee MM,Fidler SF,Shields SK,Chosay JG

doi

10.1002/jlb.60.1.27

subject

Has Abstract

pub_date

1996-07-01 00:00:00

pages

27-36

issue

1

eissn

0741-5400

issn

1938-3673

journal_volume

60

pub_type

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