Properdin Is a Modulator of Tumour Immunity in a Syngeneic Mouse Melanoma Model

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, an 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 myeloid-derived suppressor cells (MDSCs) 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.

Automated summary

Mice deficient in Properdin showed fewer myeloid-derived suppressor cells in their tumors and spleens, as well as decreased levels of M2 type macrophages and C5a, sC5b-9, and CCL2 in the serum compared to wildtype mice.