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Purpose <p>Biliary atresia (BA) has potential immune-mediated pathogenesis involving CD4 + Th1 and Th17 cells. We therefore examined antigen-presenting cells to elucidate their etiopathogenetic mechanisms.</p> Methods <p>This study cohort included 17 patients with BA and 15 controls (8 normal controls [NCs] and 7 clinical inflammation controls [CICs]). We focused on CD86<sup>+</sup> macrophages, which are antigen-presenting cells. We performed double immunohistochemistry for CD86/CD68, with double-positive and CD68-single-positive cells representing M1 and non-M1 macrophages, respectively. Macrophage subsets were morphometrically analyzed in the hepatic lobule (HL), portal area (PA), and interface (IF) and investigated in relation to clinical data.</p> Results <p>In the BA group, M1 macrophages in all regions and non-M1 macrophages in the IF and PA were significantly increased compared to those in the NC group. Notably, M1 macrophages often clustered in the IF, and non-M1 macrophages in the PA showed a small spindle-shaped morphology. Non-M1 macrophages in the IF showed a significant positive correlation with alanine aminotransferase, direct bilirubin, and fibrotic area.</p> Conclusions <p>M1 macrophages were detected as the major population in the HL and IF in BA, whereas non-M1 macrophages in the PA were correlated with hepatic fibrosis. CD86<sup>+</sup> and CD86<sup>−</sup> macrophages immunologically distinguish HL with IF from PA in BA.</p>

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Macrophage subtypes distinguish the hepatic lobule from portal area as sites of inflammation and fibrosis in liver of patients with biliary atresia

  • 期刊论文

  • 发表日期：

    2026年5月11日

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  • Yudai Tsuruno,
  • Toshihiro Muraji,
  • Haruo Ohtani,
  • Ryuta Masuya,
  • Koshiro Sugita,
  • Miki Tohma,
  • Toshihiro Yanai,
  • Yumiko Tabata,
  • Nanako Nishida,
  • Chihiro Kedoin,
  • Ayaka Nagano,
  • Masakazu Murakami,
  • Keisuke Yano,
  • Shun Onishi,
  • Toshio Harumatsu,
  • Takafumi Kawano,
  • Yuko Bitoh,
  • Satoshi Ieiri

摘要

Purpose

Biliary atresia (BA) has potential immune-mediated pathogenesis involving CD4 + Th1 and Th17 cells. We therefore examined antigen-presenting cells to elucidate their etiopathogenetic mechanisms.

Methods

This study cohort included 17 patients with BA and 15 controls (8 normal controls [NCs] and 7 clinical inflammation controls [CICs]). We focused on CD86+ macrophages, which are antigen-presenting cells. We performed double immunohistochemistry for CD86/CD68, with double-positive and CD68-single-positive cells representing M1 and non-M1 macrophages, respectively. Macrophage subsets were morphometrically analyzed in the hepatic lobule (HL), portal area (PA), and interface (IF) and investigated in relation to clinical data.

Results

In the BA group, M1 macrophages in all regions and non-M1 macrophages in the IF and PA were significantly increased compared to those in the NC group. Notably, M1 macrophages often clustered in the IF, and non-M1 macrophages in the PA showed a small spindle-shaped morphology. Non-M1 macrophages in the IF showed a significant positive correlation with alanine aminotransferase, direct bilirubin, and fibrotic area.

Conclusions

M1 macrophages were detected as the major population in the HL and IF in BA, whereas non-M1 macrophages in the PA were correlated with hepatic fibrosis. CD86+ and CD86− macrophages immunologically distinguish HL with IF from PA in BA.