Serum amyloid A delivers retinol to intestinal myeloid cells to promote adaptive immunity

Author:

Bang Ye-Ji1ORCID,Hu Zehan1ORCID,Li Yun1ORCID,Gattu Sureka1ORCID,Ruhn Kelly A.1ORCID,Raj Prithvi1ORCID,Herz Joachim2345ORCID,Hooper Lora V.16ORCID

Affiliation:

1. Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

2. Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

3. Center for Translational Neurodegeneration Research, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

4. Department of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

5. Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

6. Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

Abstract

SAAving vitamin A–mediated immunity The vitamin A metabolite retinol is critical for B and T cell development and homing to the gut. Intestinal myeloid cells such as dendritic cells and macrophages take up retinol and process it into retinoic acid (RA), which in turn initiates RA-dependent gene expression programs in lymphocytes. Bang et al . identified LDL receptor-related protein 1 (LRP1) as a myeloid cell surface receptor for retinol. LRP1 binds retinol chaperoned by serum amyloid A (SAA) proteins, and SAA–retinol complexes are then endocytosed and metabolized by myeloid cells. Mice lacking either Saa or myeloid-specific Lrp1 exhibited profound impairments in vitamin A–mediated immunity. B and T cell trafficking to the intestine, immunoglobulin A production by B cells, and protection from enteric Salmonella Typhimurium infection were all diminished when either of these crucial players was missing. —STS

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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