Redistributions of macrophages expressing the macrophage galactose-type C-type lectin (MGL) during antigen-induced chronic granulation tissue formation.
Cell surface lectins are known to regulate trafficking of cells in the immune system, yet the role of macrophage galactose-type C-type lectin 1 and 2 (MGL1/2) is poorly understood. In this study, antigen-specific chronic inflammation was induced in a subcutaneous air pouch model in mice, and distribution of cells expressing MGL1/2 was investigated. Azobenzenearsonate-conjugated acetylated BSA, used as an antigen, was introduced into an air pouch of immunized mice, and tissue formation and distribution of MGL1/2-positive cells in the sub-dermal regions was examined. Thickness of the inflammatory tissue and number of MGL1/2-positive cells simultaneously reached the maximum at day 4 and returned to the control level at day 6 or 8. When additional antigenic challenges were given, a chronic granulation tissue, which had two distinct layers, was generated. In the chronic tissue, CD11b-positive/MGL1/2-negative cells were abundant in the area close to the antigenic stimulus, while the area far from the antigenic stimulus was dominated by MGL1/2-positive/CD11b-negative or -low cells. Flow cytometric analyses of isolated cells from the granulation tissue revealed that MGL1/2-positive cells expressed MHC class II at high levels, CD11b at low levels but no CD11c. MGL1/2-positive and -negative fractions were separated from cells in the granulation tissue and a higher level of IL-1alpha messenger RNA than negative populations was detected in the MGL1/2-positive fraction by the semi-quantitative reverse transcription-PCR method. IL-1alpha production by MGL1/2-positive cells was also immunohistochemically detected. Results suggest that MGL1/2-positive cells represent a distinct sub-population of macrophages, having unique functions in the generation and maintenance of granulation tissue induced by antigenic stimuli.
Sato
Kayoko
K
Laboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Imai
Yasuyuki
Y
Higashi
Nobuaki
N
Kumamoto
Yosuke
Y
Mukaida
Naofumi
N
Irimura
Tatsuro
T
D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D001212:Asialoglycoproteins / Q000032:analysis / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D005690:Galactose / Q000378:metabolism; D006097:Granulation Tissue / Q000166:cytology / Q000276:immunology*; D007114:Immunization; D007375:Interleukin-1 / Q000378:metabolism; D037181:Lectins, C-Type / Q000032:analysis / Q000378:metabolism*; D008264:Macrophages / Q000276:immunology*; D008565:Membrane Proteins / Q000032:analysis / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D010641:Phenotype; D048069:Tumor Necrosis Factors / Q000378:metabolism
D015703:Antigens, CD; D001212:Asialoglycoproteins; C064720:Clec10a protein, mouse; D007375:Interleukin-1; D037181:Lectins, C-Type; C464940:MGL2 protein, mouse; D008565:Membrane Proteins; D048069:Tumor Necrosis Factors; D005690:Galactose