Properdin is a modulator of tumour immunity in a syngeneic mouse melanoma model

Lee Machado*, Izzat Abdulsatar Mezher Al-Rayahi, Cordula Stover

*Corresponding author for this work

Research output: Contribution to JournalArticlepeer-review

Abstract

Background and objectives: Tumours are often low immunogenic. The role of complement, an innate immune defence system, in tumour control has begun to be elucidated, but findings are conflicting. A role for properdin, amplifier of complement activation, in tumour control has recently been implicated. Materials and Methods: Properdin-deficient and congenic wildtype mice were injected subcutaneously with B16F10 melanoma cells. Tumour mass and chemokine profile were assessed. The frequencies of CD45+CD11b+ Gr-1+ cells were determined from tumours and spleens, and CD206+ F4/80+ cells were evaluated in spleens. Sera were analysed for C5a, sC5b-9 and CCL2. Results: Whilst there was no difference in tumour growth at study endpoint, properdin-deficient mice had significantly fewer MDSC in their tumours and spleens. Splenic M2 type macrophages and serum levels of C5a, sC5b-9 and CCL2 were decreased in properdin deficient compared to wildtype mice. Conclusions: The presence of intact complement amplification sustains an environment that lessens potential anti tumour responses.
Original languageEnglish
JournalMedicina
DOIs
Publication statusPublished - 21 Jan 2021

Keywords

  • CCL2
  • MDSC
  • Melanoma
  • B16

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