title: Phenotype for activated tissue macrophages in histiocytic necrotizing lymphadenitis.
abstract: Macrophage polarization is divided into M1 and M2 type based on membrane receptors, cytokines, and chemokines. M1 expresses CD80, interleukin (IL)-6, IL-12, and chemokine receptor (CCR)7, while M2 expresses CD163, IL10, and chemokine ligand (CCL)22. The aim of the present study was to identify the properties of infiltrating tissue macrophages in histiocytic necrotizing lymphadenitis (HNL). Twenty patients with HNL were studied, and immunohistochemistry for CD68 (KP1), CD163, CCL22, CCR7, and CD123 was done, along with myeloperoxidase (MPO). To evaluate the phenotypes of tissue macrophages in HNL, the number of cells stained positively for CD163, CCL22, CCR7, CD123 and MPO concurrently with CD68 was counted, and the ratio was calculated for each antibody to CD68+ cells. There was a high rate of co-expression for CD163 (median, 78%) or CCL22 (80%) and a low rate for CCR7 (5%) in CD68+ cells. It is therefore conceivable that infiltration by M2 macrophages is dominant in HNL. Furthermore, some CD68+ tissue macrophages in HNL co-express MPO or CD123 (range, 5-80%; median, 23% and 40%, respectively). It is suggested that these characteristic tissue macrophages may be associated with the pathogenesis of HNL and that M2 macrophages may infiltrate to repair the lymphoid tissue injured by cytotoxic T cells in HNL.
authors.affiliation: Department of Pathology, School of Medicine, Kurume University, Kurume 830-0011, Japan. yuko-nomura@mvj.biglobe.ne.jp
authors.forename: Yuko
authors.initials: Y
authors.lastname: Nomura
authors.forename: Masanori
authors.initials: M
authors.lastname: Takeuchi
authors.forename: Shiro
authors.initials: S
authors.lastname: Yoshida
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Sugita
authors.forename: Daisuke
authors.initials: D
authors.lastname: Niino
authors.forename: Yoshizo
authors.initials: Y
authors.lastname: Kimura
authors.forename: Kei
authors.initials: K
authors.lastname: Shimizu
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Aoki
authors.forename: Nobuko
authors.initials: N
authors.lastname: Suefuji
authors.forename: Shinichi
authors.initials: S
authors.lastname: Hirose
authors.forename: Masahiro
authors.initials: M
authors.lastname: Kikuchi
authors.forename: Koichi
authors.initials: K
authors.lastname: Ohshima
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D002648:Child; D005260:Female; D020042:Histiocytic Necrotizing Lymphadenitis / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D053650:Interleukin-3 Receptor alpha Subunit / Q000378:metabolism; D008198:Lymph Nodes / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009195:Peroxidase / Q000378:metabolism; D010641:Phenotype; D055815:Young Adult; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015415:Biomarkers; D053650:Interleukin-3 Receptor alpha Subunit; D009195:Peroxidase; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C115022:IL3RA protein, human