Three major subsets of Ag-experienced CD8+ T cells have been identified according to their expression of CD62L and CD127 These markers are associated with central memory T cells (CD62L+ CD127+), effector memory T cells (CD162L- CD127+), and effector T cells (CD62L- CD127-) In this study we characterized the development of these three populations during acute and chronic viral infections and after immunization with virus-like particles and determined their lineage relation and functional and protective properties We found that the balance between the three subsets was critically regulated by the availability of Ag and time After initial down-regulation of CD127, the responding CD8+ T cell population down-regulated CD62L and re-expressed CD127 Dependent on Ag availability, the cells then further differentiated into CD62L- CD127- effector cells or, in the absence of Ag, re-expressed CD62L to become central memory T cells Although all three populations efficiently produced effector cytokines such as IFN-gamma, CD62L- CD127- effector cells exhibited the highest ex vivo lytic potential In contrast, CD62L+ CD127+ central memory T cells most efficiently produced IL-2 and proliferated extensively in vitro and in vivo upon antigenic restimulation Strikingly, only effector and effector memory, but not central memory, T cells were able to protect against peripheral infection with vaccinia virus, whereas central memory T cells were most potent at protecting against systemic infection with lymphocytic choriomeningitis virus, indicating that the antiviral protective capacities of specific CD8+ T cell subsets are closely related to the nature of the challenging pathogen

Functional Properties and Lineage Relationship of CD8+ T Cell Subsets Identified by Expression of IL-7 Receptor α and CD62L

Increased TCR avidity after T cell activation: a mechanism for sensing low-density antigen.

Whether there is one or multiple αβT cell antigen receptor (TCR) recognition modules in a given TCR/CD3 complex is a long-standing controversy in immunology. We show that T cells from transgenic mice that coexpress comparable amounts of two distinct TCRβ chains incorporate at least two αβTCRs in a single TCR/CD3 complex. Evidence for bispecific αβTCRs was obtained by immunoprecipitation and immunoblotting and confirmed on the surface of living cells both by fluorescence resonance energy transfer and comodulation assays by using antibodies specific for TCRβ-variable regions. Such (αβ)2TCR/CD3 or higher-order complexes were evident in T cells studied either ex vivo or after expansion in vitro. T cell activation is thought by many, but not all, to require TCR cross-linking by its antigen/major histocompatibility complex ligand. The implications of a multivalent (αβ)2TCR/CD3 complex stoichiometry for the ordered docking of specific antigen/major histocompatibility complex, CD4, or CD8 coreceptors and additional TCRs are discussed.

Multivalent structure of an αβT cell receptor

A correlation between tcr valpha docking on mhc and cd8 dependence: implications for t cell selection

https://www.cell.com/immunity/pdf/S1074-7613(03)00269-3.pdf

A Correlation between TCR Vα Docking on MHC and CD8 Dependence: Implications for T Cell Selection

T cell activation involves specific interactions between the TCR and peptides presented by the MHC. This engagement leads to phosphorylation and subsequent internalization of the TCR complex. By analyzing the kinetics of the internalization of TCR, we found that the rate of TCR down-regulation was proportional to the square of the TCR density. Mathematical modeling of TCR interactions indicates that such a relation is only possible if TCR dimerize before internalization. By mathematical analysis, our data would also be compatible with trimer but not larger oligomer formation. Thus, minimal TCR oligomerization is an essential step for peptide-mediated T cell activation.

Formation of TCR dimers/trimers as a crucial step for T cell activation

The role of T cell receptor dimerization for T cell antagonism and T cell specificity.

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Formation of TCR dimers/trimers as a crucial step for T cell activation

The role of T cell receptor dimerization for T cell antagonism and T cell specificity.