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<i>Background and Objectives</i>: 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. <i>Materials and Methods</i>: 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. <i>Results</i>: 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. <i>Conclusions</i>: The presence of intact complement amplification sustains an environment that lessens potential anti-tumour responses.