The reduced levels of these molecules suggest that (i) the progenitor’s entry into the thymus and migration could be compromised; (ii) the control of the infection in the thymus, mediated by recirculation of mature SP CXCR3+ peripheral T cells back to the thymus could be also compromised; (iii) the increase of Ccr7 and Cd62l levels on thymocytes from malnourished animals concomitant with the accumulation SP cells observed on these animals, reinforce the hypothesis that protein malnutrition has a deleterious defect on thymocyte migration. This evidence concerns the gene SELL and infection.