The co-evolution of pathogens and their target hosts has led to the establishment of close and complex interactions between them. From protozoa to moulds, the interactions set up during host colonisation allow the parasite to escape or even to control the host to divert its resources, which can lead to cell exhaustion and programmed cell death for the benefit of the parasite. Throughout my scientific career, I have been lucky enough to be part of several research teams interested, as I was, in understanding the ability of parasites to manipulate the biology of their host cell and the danger signals it triggers. Thus, during my master's and doctoral studies, and my postdoctoral position, I studied intracellular protozoa such as Neospora caninum and Plasmodium sp. After my recruitment as associate professor at the EnvA, I wanted to apply the knowledge acquired in the understanding of the cellular interaction between the mould Aspergillus fumigatus and the cells responsible for the first line of lung defence. While Neospora is responsible for the severe economic losses associated with abortion in cattle, Plasmodium infection continues to have devastating consequences for the health and livelihoods of people around the world. The intracellular nature of these two parasites is an example of their ability to camouflage themselves from host defence mechanisms at the cellular and immune level. In the first part of this paper, I show the importance of regulating the expression of parasitic surface proteins and those produced by secretory vesicles during the invasion and transformation within the host cell, such as SAG1 and BSR4 in Neospora, or PLP1 and RON4 in Plasmodium. The characterisation and manipulation of the genes expressing these proteins has allowed the development of strategies for the early diagnosis and/or prevention of infection. While host cell manipulation is an expected mechanism in intracellular protists, this ability is not well known in other eukaryotes such as the mould Aspergillus fumigatus. This opportunistic fungus is capable of causing various forms of mycosis in humans and animals. Thus, aspergillosis can be responsible for disabling and even fatal respiratory disorders and serious economic losses in the poultry sector. In the second part of this paper, I explain how the outcome of aspergillosis infection depends on early innate response mechanisms activated in two avian hosts by molecular patterns associated with the surface of A. fumigatus. The stimulation of the pro-inflammatory response, but also the production of certain immunoglobulins appears to be essential to ensure colonisation of the respiratory parenchyma to the detriment of its function in the affected birds, with varying degrees of success depending on the affected avian species. Finally, in the research team that I have just joined within the UMR-BIPAR (ANSES, EnvA, INRAe), I will continue with this co-evolutionary approach, but this time by exploring the more complex interaction between a protozoan (Babesia) and its vector (Ixodidae tick). I will take advantage of the cutting-edge tools and techniques developed by my team to analyse their cellular interactions and propose means of controlling and preventing piroplasmosis, a scourge for animal health and a growing public health concern worldwide.