Eimeria, an obligatory intracellular parasite, is the causal agent of coccidiosis. Among seven species, Eimeria tenella is one of the most pathogenic and leads to high economic impact in poultry industry. It colonizes the caecum leading to lesions and to an inappropriate inflammatory response. Neutralization of the pro‐inflammatory IL‐17A leads to the decrease of oocysts shedder, parasite migration in the lamina propria and lesionnal scoring in the caeca (Del Cacho et al. 2014). Several types of lymphocytes can produce IL‐17A, one of the stronger cell producer being the γδ T‐cells. To better understand the physiopathology of caecal coccidiosis and the importance of γδ T‐cells, we investigated the presence of γδ T‐cell in the caeca of chickens at homeostasis and during Eimeria tenella infection. Our results show an increase in the number of leukocytes and γδ T‐cells with the infection but a decrease in the proportion of γδ T‐cells within leukocytes. The analysis of different mediators of inflammation on caecal tissues at 7 days post infection shows an increase in mRNAs encoding INFγ, IL‐17A and IL‐22 which are mediators synthesized by γδ T‐cells. We are now defining sub‐populations of γδ T‐cells that will be further functionally characterized. During the infection, the impact of microbiota on the physiopathology and more particularly on the γδ T‐cell subpopulations and their functional characterization will also be studied. Preliminary data have shown that Eimeria tenella associated‐lesions are dependent on the microbiota. Consequently, using axenic and conventional chickens will constitute a model for studying the importance of γδ T‐cells and their mediators on the physiopathology of the infection.