To examine this possibility, CFSE splenocytes from LPS-treated mice were transferred into recipient mice treated with Dex after the inflammatory process was triggered by LPS (Fig. 2F). Interestingly, in this experimental condition the entrance of peripheral cells into the thymus occurred. Similar data were observed when T. cruzi infected mice were used instead of LPS-treated mice find more (data not shown). Overall, these data indicate that space is necessary but not sufficient for the entrance of cells into the thymus and we hypothesize that specific signals that recruit peripheral cells into the organ are also required. To characterize the phenotype of cells that

enter the thymus during Th1-inflammatory/infectious processes, we analyzed the expression of markers that discriminate between naïve, recently act-ivated or memory T cells (CD44, CD62L, Selleckchem Pexidartinib and CD69). Data shown in Fig. 3A demonstrate that cells that enter the thymus exhibited high expression of CD44 and CD62L but low expression of CD69. Together, cells migrating to the thymus exhibited surface expression markers compatible with a central memory phenotype. It has been demonstrated that traffic of peripheral B and T cells to the thymus in AKR mouse is mediated by the expression of L-selectin

on immigrating lymphocytes [11]. Thus, we analyzed CD62L expression in all the cell types recruited to the thymus in LPS-treated and T. cruzi infected mice. As shown in Fig. 3B, CD62L was expressed by most immigrating B and CD4+ T cells and about 70% of CD8+ lymphocytes,

suggesting that the integrin could represent an important pathway for cells to extravasate into the thymus. However, data presented in Fig. 3C demonstrate that CD62L is not involved Dichloromethane dehalogenase in cell migration to the thymus since splenocytes from LPS-treated mice incubated with an anti-CD62L neutralizing Ab before the adoptive transfer did not affect migration of either mature T or B cells to the thymus (Fig. 3C), but highly diminished the entrance of transferred cells to popliteal LNs (data not shown) [28]. Similar results were found in the LPS model (data not shown). did not participate in the entry of mature lymphocytes into the thymus, we focused our attention on other integrin/chemokines candidates. We found that the expression of the chemokine MCP-1 was highly upregulated in the thymi of LPS-treated, C. albicans, or T. cruzi infected mice compared with that of controls (Fig. 4A). Ex vivo treatment of thymocytes from T. cruzi infected mice with Brefeldin A for 4 h and then intracellular staining with an anti-MCP-1 Ab demonstrated a low but consistent detection of MCP-1+ cells (Supporting Information Fig. 1). The expression of MCP-1 was mainly restricted to B and CD4+ and CD8+ CD44lo resident thymocytes, but not to CD44hi peripheral T-cell counterparts or CD11b+ and CD11c+ subsets (Supporting Information Fig. 1).