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 conflicting. A for properdin, amplifier complement activation, recently been implicated. Materials Methods: Properdin-deficient congenic wildtype mice were injected subcutaneously with B16F10 melanoma cells. Tumour mass chemokine profile assessed. frequencies CD45+CD11b+ Gr-1+ cells determined from tumours spleens, CD206+ F4/80+ evaluated spleens. Sera analysed C5a, sC5b-9, CCL2. Results: Whilst there was no difference growth at study endpoint, properdin-deficient had significantly fewer myeloid-derived suppressor (MDSCs) their Splenic M2 type macrophages serum levels CCL2 decreased compared mice. Conclusions: presence intact amplification sustains environment that lessens potential anti-tumour responses.