Phenotypic and functional profiles of CRIg (Z39Ig)-expressing macrophages in the large intestine

Innate Immun. 2012 Apr;18(2):258-67. doi: 10.1177/1753425911400641. Epub 2011 Jul 18.

Abstract

Intestinal macrophages (Mφ) play significant roles in maintaining homeostasis by the efficient elimination of foreign particles in the large intestine. However, functional complement receptors have not been fully identified. In this study, we showed that a complement receptor of the Ig superfamily (CRIg, also known as Z39Ig), a receptor for complement fragments (C3b and iC3b), was expressed on a subset of intestinal M in murine and human large intestine. When abilities of uptake of antigens of murine CRIg(+) Mφ were examined, intestinal CRIg(+) Mφ displayed less endocytic and similar phagocytic abilities compared to resident peritoneal F4/80(+)CRIg(-) Mφ and F4/80(+)CRIg(+) Mφ. Additionally, we found that a significant portion of C3b-dependent phagocytosis by large intestinal M involves CRIg, emphasizing the importance of efficient mechanisms to eliminate foreign particles in the large intestine. On the other hand, intestinal Mφ from 2,4,6-trinitrobenzene sulfonic acid-treated mice had decreased CRIg expression but increased CD11b expression, implying some contribution to the removal of immune complexes. This study will shed new light on opsonization and phagocytosis by large intestinal Mφ.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD11b Antigen / metabolism
  • Cell Separation
  • Colitis / pathology
  • Complement C3b / metabolism
  • Female
  • Flow Cytometry
  • Humans
  • Immunohistochemistry
  • Intestine, Large / cytology*
  • Intestine, Large / physiology*
  • Macrophages / physiology*
  • Macrophages, Peritoneal / physiology
  • Mice
  • Mice, Inbred BALB C
  • Phagocytosis
  • Phenotype
  • Receptors, Complement / physiology*
  • Receptors, Complement 3b / physiology*

Substances

  • CD11b Antigen
  • CR1 protein, human
  • Receptors, Complement
  • Receptors, Complement 3b
  • VSIG4 protein, mouse
  • Complement C3b