As CD8+ TEM cells persist long-term in the liver (Figure 1), we asked whether these persisting CD8+ TEM cells could also be detected in peripheral blood. CD8+ TEM were found in the blood 8 weeks after challenge and the TCR Vβ profile was the same as that observed 1 week after challenge. Thus, it appears
that once the commitment is made to the expression of a given TCR Vβ repertoire, this expression is maintained long-term. Moreover, the reduced frequency and number of CD8+ TEM observed in the liver 8 weeks after challenge (Table 1) is not because of a selective loss of any TCR Vβ family, but rather a general loss of all CD8+ TEM cells, as would be expected during the contraction phase that occurs after infection. To determine whether any particular Selleckchem Crizotinib TCR Vβ is more likely to be expanded in TEM cells, we combined the data from 43 mice (28 analysed in liver, 15 analysed in blood). Results in Figure 7 display the ratio of TCR Vβ expression by CD8+ TEM over CD8+ TN cells, and it represents the expansion or contraction of TEM cells in individual mice. Using an arbitrary cut-off point of CAL-101 research buy 2, the CD8+ TEM cells from at least one mouse analysed had an expansion of a particular TCR Vβ family, except for Vβ3. In addition, some TCR Vβ were more likely to be expanded than others, and common among these were Vβ8.3 (26% of mice), Vβ6 (21%), Vβ7 (16%),
Vβ9 (16%), Vβ11 (16%) or Vβ4 (14%). In this study, we characterized the TCR Vβ usage by intrahepatic and blood CD8+ T cells during Pbγ-spz immunization
and challenge of C57BL/6 mice. The liver and blood Ixazomib of unimmunized mice contain very few CD8+ TEM cells but they appear after immunization with γ-spz and increase after challenge with infectious spz. The repertoire CD8+ TN and TCM cells was diverse and it was conserved between individual mice, and did not change with immunization. In contrast, preferential usage of one or more TCR Vβ subset was observed in CD8+ TEM cells after immunization. The particular expanded TCR Vβ varied between individual mice but Vβ4, 6, 7, 8.3, 9 and 11 were the most frequent. In the majority of malaria-related studies, the usage of TCR Vβ chain is usually associated with the pathogenesis of Plasmodia infections. Development of P. berghei cerebral malaria during blood-stage infection is associated with oligoclonal TCR Vβ4, 8.1 and 11 CD8+ T cells in the brains of affected C57BL/6 mice (32,33). In another study, cerebral malaria in B10.D2 mice is associated with an increase in CD8+ peripheral blood lymphocytes (PBLs) expressing Vβ8.1,8.2 (34). In contrast, the Vβ distribution on CD3+ PBLs was not different between patients with malaria (uncomplicated or cerebral malaria) and asymptomatic controls in a cohort of African children (35).