Compared to the previously limited data on genetic correlations between ITs in pigs, our study provides a large-scale estimation of phenotypic and genetic correlations among 32 ITs. PCA results and correlation estimations highlight the weak phenotypic and genetic correlations between the different ITs, except mainly for cell subsets. No cluster of innate and adaptive ITs is revealed. These results illustrate that many of the ITs included in our study provide more or less independent potential clues for selecting for improved immunocompetence. Such complementarity is expected since innate immunity is in place or ready for activation prior to infection or antigenic stimulation and collaborates with adaptive immunity, which is induced by infection or antigenic stimulation. Nevertheless, a few highly positive genetic correlations have been detected between total number of white blood cells and some leukocytes subsets, and between some leukocyte subsets such as total number of lymphocytes, CD4 -CD8 + lymphocytes (which contains ab CD4 -CD8 + lymphocytes and NK), and NK cells (CD16 + CD2 + cells). Phagocytosis, production of IL8 and TNF, two pro-inflammatory cytokines produced by monocytes and macrophages, were positively correlated with acute inflammatory phase proteins produced by hepatocytes i.e. CRP and HAPT. A high correlation was also found between CRP and HAPT. Clapperton and colleagues [17] have shown that phenotypic correlations between leukocyte subsets and acute phase proteins are weak (,0.2) and not significantly different from zero in agreement with our results. In contrast to our study, Clapperton and collaborators have not detected any significant genetic and phenotypic correlations between different leukocyte subsets except when one subset was nested in another [16] .