Cutting Edge: Stimulation with the Cognate Self-Antigen Induces Expression of the Ly49A Receptor on Self-Reactive T Cells Which Modulates Their Responsiveness

Saurer, Leslie; Seibold, Inge; Vallan, Claudio; Held, Werner; Mueller, Christoph

doi:10.4049/jimmunol.171.12.6334

Cited by 6 publications

(8 citation statements)

References 20 publications

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“…This hypothesis is supported by the induction of Ly49A on alloreactive mouse CD8 ϩ T cells upon persistent exposure to the Ag (53), as well as by the KIR ϩ CD8 ϩ T cell expansions upon bone marrow transfer in human (54). Our results obtained in the HY-specific model are also consistent with the recently reported induction of Ly49 on self-reactive CD8 Ϫ T cells (55). Yet, it remains to be investigated whether the induction of Ly49 ϩ on T cells is restricted to self-reactive T cells, or whether these circumstances of persistent stimulation also occur upon exogenous challenges.…”

Section: Cd8supporting

confidence: 80%

Expansion and Function of CD8+ T Cells Expressing Ly49 Inhibitory Receptors Specific for MHC Class I Molecules

Anfossi

Robbins

Ugolini

et al. 2004

The Journal of Immunology

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MHC class I-specific Ly49 inhibitory receptors regulate NK cell activation, thereby preventing autologous damage to normal cells. Ly49 receptors are also expressed on a subset of CD8+ T cells whose origin and function remain unknown. We report here that, despite their phenotypic and cytolytic similarities, Ly49+CD8+ T cells and conventional Ly49−CD44high memory-phenotype CD8+ T cells present strikingly distinct features. First, under steady state conditions Ly49+CD8+ T cells are poor cytokine producers (TNF-α and IFN-γ) upon TCR triggering. Second, Ly49+CD8+ T cells are not induced upon various settings of Ag immunization or microbial challenge. However, Ly49 can be induced on a fraction of self-specific CD8+ T cells if CD4+ T cells are present. Finally, the size of the Ly49+CD8+ T cell subset is selectively reduced in the absence of STAT1. These results indicate that Ly49 expression is associated with a differentiation program of cytolytic CD8+ T cells triggered upon chronic antigenic exposure. They further suggest that the size of the Ly49+CD8+ T cell subset marks a history of CD8+ T cell activation that might preferentially result from endogenous inducers of inflammation rather than from microbial infections.

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Section: Cd8supporting

confidence: 80%

Expansion and Function of CD8+ T Cells Expressing Ly49 Inhibitory Receptors Specific for MHC Class I Molecules

Anfossi

Robbins

Ugolini

et al. 2004

The Journal of Immunology

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“…Although the Ly49 + CD8 T-cell pool is incomparably smaller than of the conventional CD8 T-cells and contracts faster, the antigen-specific Ly49 + CD8 T-cells are detectable even 24 days post-infection. We also observed the broad antigen specificity of Ly49 + CD8 T-cells generated during the infection ( Figures 4E and S2B ), which agrees with the polyclonal nature of Ly49 + CD8 T-cells ( 8 , 16 ). We did not perform more extensive experiments to assess the effector functions of Ly49 + CD8 T-cells due to the limited number of this cell population even during the infection.…”

Section: Discussionsupporting

confidence: 84%

“…The major factors affecting the upregulation of Ly49 receptors by CD8 T-cells include the immune response and STAT1 signaling ( 10 , 13 , 15 , 16 , 31 ). Immunization with MHC class II-restricted antigens also facilitates the upregulation of Ly49 receptors on CD8 T-cells, which suggests interactions with some other cells, presumably with activated T-cells ( 11 , 12 , 30 ).…”

Section: Discussionmentioning

confidence: 99%

Functional Characterization of Ly49+CD8 T-Cells in Both Normal Condition and During Anti-Viral Response

Shytikov

Rohila

et al. 2021

Front. Immunol.

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The role of Ly49+CD8 T-cells in the immune system is not clear. Previously, several papers suggested Ly49+CD8 T-cells as immunosuppressors, while multiple studies also suggested their role as potent participants of the immune response. The mechanism of Ly49 expression on CD8 T-cells is also not clear. We investigated phenotype, functions, and regulation of Ly49 expression on murine CD8 T-cells in both normal state and during LCMV infection. CD8 T-cells express different Ly49 receptors compared with NK-cells. In intact mice, Ly49+CD8 T-cells have a phenotype similar to resting central memory CD8 T-cells and do not show impaired proliferation and cytokine production. Conventional CD8 T-cells upregulate Ly49 receptors during TCR-induced stimulation, and IL-2, as well as IL-15, affect it. At the same time, Ly49+CD8 T-cells change the Ly49 expression profile dramatically upon re-stimulation downregulating inhibitory and upregulating activating Ly49 receptors. We observed the expression of Ly49 receptors on the virus-specific CD8 T-cells during LCMV infection, especially marked in the early stages, and participation of Ly49+CD8 T-cells in the anti-viral response. Thus, CD8 T-cells acquire Ly49 receptors during the T-cell activation and show dynamic regulation of Ly49 receptors during stimulation.

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“…However, expression of Ly49 receptors was not observed on CD44 high CD8 ϩ T cells arising following the transfer of naive donor CD8 ϩ T cells into lymphopenic hosts (29). Nevertheless, a recent paper describes the induction of Ly49A expression upon CD8 Ϫ T cells arising from a CD8 ϩ population in mice dual-transgenic for the LCMV-derived gp33 peptide and a TCR specific for gp33 (30). Up-regulation of Ly49A expression on these self-reactive CD8 ϩ T cells substantially reduced their activation upon encounter with their cognate self-Ag.…”

Section: Discussionmentioning

confidence: 99%

Origin and Fate of Lymphocytic Choriomeningitis Virus-Specific CD8+ T Cells Coexpressing the Inhibitory NK Cell Receptor Ly49G2

Peacock

Welsh

2004

The Journal of Immunology

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CD8+ T cells that coexpress the inhibitory NK cell receptor, Ly49G2 (G2), are present in immunologically naive C57BL/6 mice but display Ags found on memory T cells. To assess how G2+CD8+ cells relate to bona fide memory cells, we examined the origin and fate of lymphocytic choriomeningitis virus (LCMV)-induced G2+CD8+ cells. During early (day 4) acute LCMV infection, both G2+ and G2−CD8+ T cell subsets underwent an attrition in number and displayed an activation (CD69high1B11highCD62Llow) phenotype. By day 8, both subsets synthesized IFN-γ in response to immunodominant LCMV peptides, though the expansion of G2+ cells was less than that of G2− cells. Adoptive transfer experiments with purified G2− or G2+CD8+ cells from naive mice indicated that the LCMV-specific G2+ subset was derived from a pre-existing G2+ population and not generated from G2− cells responding to LCMV infection. Their participation in the LCMV-specific T cell response increased with age, reflecting an increase in the size of the pre-existing G2+ pool. Following establishment of stable LCMV memory, the proportion of CD8+ cells coexpressing G2 was reduced in comparison to naive controls, presumably due to displacement by G2− LCMV-specific memory cells. LCMV-specific G2+ cells were present in the memory pool, but at low frequencies, and they did not exhibit the typical phenotypic changes of reactivation during secondary challenge. We suggest that G2+CD8+ cells represent a cell lineage distinct from bona fide memory T cells, but that they can participate in an acute virus-specific T cell response.

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Cutting Edge: Stimulation with the Cognate Self-Antigen Induces Expression of the Ly49A Receptor on Self-Reactive T Cells Which Modulates Their Responsiveness

Cited by 6 publications

References 20 publications

Expansion and Function of CD8+ T Cells Expressing Ly49 Inhibitory Receptors Specific for MHC Class I Molecules

Expansion and Function of CD8+ T Cells Expressing Ly49 Inhibitory Receptors Specific for MHC Class I Molecules

Functional Characterization of Ly49+CD8 T-Cells in Both Normal Condition and During Anti-Viral Response

Origin and Fate of Lymphocytic Choriomeningitis Virus-Specific CD8+ T Cells Coexpressing the Inhibitory NK Cell Receptor Ly49G2

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