Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2000 Jul 17;192(2):205–218. doi: 10.1084/jem.192.2.205

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2000 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Marked neutrophilic inflammation in mice deficient in CCR2. (A) The histopathological sections (hematoxylin and eosin; original magnification: ×400) are from mice infected for 5 wk with L. major. Abundant organisms admixed with areas of necrosis, karryohectic cellular fragments, and polymorphonuclear leukocytes including eosinophils were found in CCR2^−/− mice. In contrast, the ears from +/+, CCR5^−/−, and MIP-1α^−/− mice had fibroblasts with scattered cellular infiltrates that consisted of mononuclear cells, epitheloid histiocytes, lymphocytes, and plasmacytoid cells. Necrosis was absent in these three groups of mice. (B) Marked recruitment of neutrophils to the ears of CCR2-null mice after intradermal infection with L. major. 1 and 7 d after L. major infection, the cells that emigrated from ear skin explants were stained with FITC-labeled anti-I-A^b mAb and PE-labeled anti–Ly-6G mAb. Percentage (left) and total number (right) of neutrophils (Ly-6G brightI-A^b−) among all cells that emigrated from skin explants of +/+ (○), CCR2^−/− (•), and CCR5^−/− (▵) mice are shown. Results from one of three representative experiments are shown.

Marked neutrophilic inflammation in mice deficient in CCR2. (A) The histopathological sections (hematoxylin and eosin; original magnification: ×400) are from mice infected for 5 wk with L. major. Abundant organisms admixed with areas of necrosis, karryohectic cellular fragments, and polymorphonuclear leukocytes including eosinophils were found in CCR2^−/− mice. In contrast, the ears from +/+, CCR5^−/−, and MIP-1α^−/− mice had fibroblasts with scattered cellular infiltrates that consisted of mononuclear cells, epitheloid histiocytes, lymphocytes, and plasmacytoid cells. Necrosis was absent in these three groups of mice. (B) Marked recruitment of neutrophils to the ears of CCR2-null mice after intradermal infection with L. major. 1 and 7 d after L. major infection, the cells that emigrated from ear skin explants were stained with FITC-labeled anti-I-A^b mAb and PE-labeled anti–Ly-6G mAb. Percentage (left) and total number (right) of neutrophils (Ly-6G brightI-A^b−) among all cells that emigrated from skin explants of +/+ (○), CCR2^−/− (•), and CCR5^−/− (▵) mice are shown. Results from one of three representative experiments are shown.