Vitamin D upregulates the macrophage complement receptor immunoglobulin in innate immunity to microbial pathogens

Annabelle G. Small, Sarah Harvey, Jaspreet Kaur, Trishni Putty, Alex Quach, Usma Munawara, Khalida Perveen, Andrew McPhee, Charles S. Hii, Antonio Ferrante

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28 Citations (Scopus)
21 Downloads (Pure)


Vitamin D deficiency remains a global concern. This ‘sunshine’ vitamin is converted through a multistep process to active 1,25-dihydroxyvitamin D3 (1,25D), the final step of which can occur in macrophages. Here we demonstrate a role for vitamin D in innate immunity. The expression of the complement receptor immunoglobulin (CRIg), which plays an important role in innate immunity, is upregulated by 1,25D in human macrophages. Monocytes cultured in 1,25D differentiated into macrophages displaying increased CRIg mRNA, protein and cell surface expression but not in classical complement receptors, CR3 and CR4. This was associated with increases in phagocytosis of complement opsonised Staphylococcus aureus and Candida albicans. Treating macrophages with 1,25D for 24 h also increases CRIg expression. While treating macrophages with 25-hydroxyvitamin D3 does not increase CRIg expression, added together with the toll like receptor 2 agonist, triacylated lipopeptide, Pam3CSK4, which promotes the conversion of 25-hydroxyvitamin D3 to 1,25D, leads to an increase in CRIg expression and increases in CYP27B1 mRNA. These findings suggest that macrophages harbour a vitamin D-primed innate defence mechanism, involving CRIg.

Original languageEnglish
Article number401
Number of pages7
JournalCommunications Biology
Issue number1
Publication statusPublished - 25 Mar 2021
Externally publishedYes


  • Antimicrobial responses
  • Calcium and vitamin D
  • Infection
  • Phagocytes


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