Peripheral Lymphoid Volume Expansion and Maintenance Are Controlled by Gut Microbiota via RALDH+ Dendritic Cells. (Immunity. 2016, 16;44(2):330-42.)

報告日期: 2017/04/11
報告時間: 5:10/6:00
報告學生: 陳佩琪
講評老師: 陳振瑋
附件下載: 下載[1625-1487730047-1.pdf] 

Peripheral Lymphoid Volume Expansion and Maintenance Are Controlled by Gut Microbiota via RALDH+ Dendritic Cells

Zongde Zhang, Jianjian Li, Wencheng Zheng, Guang Zhao, Hong Zhang,

Xiaofei Wang, Yaqian Guo, Chuan Qin, and Yan Shi,Immunity (2016) 44: 330–342.

Speaker: Pei-Chi Chen (陳佩琪)                    Time : 17:10~18:00, Apr.11, 2017

Commentator: Dr. Jenn-Wei, Chen (陳振暐)    Place: Room 602

The fundamental principal of peripheral lymph nodes (pLNs) is to filter potentially harmful particles from the lymph and promote lymphocyte homing to encounter their specific antigen to initiate adaptive immunity. Since 1963, scientists had found that pLNs in germ-free (GM) mice are structureless and B cells are also rare in that of GF mice [1]. It seems that the microbiota plays a critical role in pLN developments. However, seldom research demonstrated the detail mechanism of how the microbiota regulates the development of pLNs. In this study, Zhang et al. proved that commensal fungi drive a distinct gut dendritic cells (DCs) migrating to pLNs, where these DCs instruct the maturation of high endothelial venules (HEVs), allowing lymphocytes to entry LN, and imprint peripheral lymphocytes for gut homing. In the beginning, the authors found that the greatest difference of transcritopme in pLN of GF and specific-pathogen-free (SPF) mice were associated with retinoic acid (RA) signaling. Furthermore, they established that a distinct DC population within pLNs, CD103+CD11b+DCs, also expressed retinal dehydrogenase (RALDH), was strongly reduced in LNs from GF mice in comparison to SPF mice. RALDH is the enzyme involved in RA catabolism [2]. Following experiments demonstrated that Candida tropicalis triggered migration of CD103+RALDH+DCs from intestinal lamina propria to pLNs by attraction of MAdCAM-1 on HEVs in early life. Surprisingly, this is the first study reporting CD103+RALDH+DCs could travel long distance to initiate pLN development. Besides, these DCs promoted the maturation of HEVs by converting the addressins expression from MAdCAM-1 (immature phenotype) to PANd (mature phenotype), which induces pLN development to performing their function. At least, the authors showed that CD103+RALDH+DCs from gut induced α4β7 and CCR9, key homing receptors that regulating effector T cell tropism for intestine, on effector T cells in early life through the capacity to synthesize RA. Taken together, this research unveiled the detail path of how commensal fungi regulate pLN maturations.


  1. Bauer H, Horowitz R.E., Levenson S.M., Popper H., The response of the lymphatic tissue to the microbial flora. Studies on germfree mice. Am J Pathol. 42:471-83 (1963).
  2. Hall J.A., Grainger J.R., Spencer S.P., Belkaid Y, The role of retinoic acid in tolerance and immunity. Immunity. 35:13-22 (2011).