Visualization of peptide-specific T cell immunity and peripheral tolerance induction in vivo

Kearney, Elizabeth R.; Pape, Kathryn A.; Loh, Dennis Y.; Jenkins, Marc K.

doi:10.1016/1074-7613(94)90084-1

Cited by 899 publications

(772 citation statements)

References 38 publications

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“…The results of our comparative study indicate that the initial activation and 'programming' of epitopespecific CD4 + and CD8 + T cells occur within a similar time frame during infection. These findings are in agreement with studies using CD4 + TCR transgenic T cells [4] as well as with a recent study analyzing the in vivo T cell response during viral (LCMV) infection, in which the authors also reported synchronized kinetics in the CD8 + and CD4 + T cell compartment [8].…”

Section: Discussionsupporting

confidence: 92%

“…One of the challenges encountered in the study of pathogen-specific CD4 + T cell responses is that most known pathogenderived MHC class-II restricted epitopes are subdominant, inducing the expansion of very small populations which are difficult to identify and track directly ex vivo. For this reason, experimental models based on the adoptive transfer of TCR-transgenic T cells have been established [4]. Unfortunately, results with monoclonal T cell populations, such as TCR transgenic T cells, cannot always be directly translated to endogenous antigenspecific T cell responses, which are usually characterized by a high degree of TCR polyclonality and functional heterogeneity [5,6].…”

Section: Introductionmentioning

confidence: 99%

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Differences in maintenance of CD8⁺ and CD4⁺ bacteria‐specific effector‐memory T cell populations

et al. 2003

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Our knowledge about the kinetics and dynamics of complex pathogen-specific CD8 + T cell responses and the in vivo development of CD8 + memory T cells has increased substantially over the past years; in comparison, relatively little is known about the CD4 + T cell compartment. We monitored and directly compared the phenotypical changes of pathogen (Listeria monocytogenes)-specific CD8 + and CD4 + T cell responses under conditions leading to effective and long-lasting protective immunity. We found that the general kinetics of bacteriaspecific CD8 + and CD4 + T cells during the effector and post-effector phases are synchronized. However, later during the memory phase, CD8 + and CD4 + T cell populations differ substantially. Whereas CD8 + memory T cell populations with immediate effector function are readily detectable in lymphoid and non-lymphoid tissues and remain remarkably stable in size, antigen-specific CD4 + effector-memory T cells decline continuously in frequency over time. These findings have important implications for the better understanding of the in vivo development of protective immunity towards intracellular pathogens.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Differences in maintenance of CD8⁺ and CD4⁺ bacteria‐specific effector‐memory T cell populations

et al. 2003

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“…Purified T cells containing 2.5×10 6 CD8 + TCR V § 2 + V g 5.1 + (OT-I) or CD4 + TCR V § 2 + V g 5.1 + (OT-II) were injected i.v. into the tail vein of recipient mice [32]. After 24 h, mice were injected s.c. with 2 mg OVA ( Sigma Chemical Co., St. Louis, MO) and 50 ?…”

Section: Adoptive Transfermentioning

confidence: 99%

“…Using an adoptive transfer approach to study T cell activation in vivo [32], we compared the effects of 4-1BBL deficiency on OT-I (CD8, MHC class I-restricted T cells) and OT-II (CD4, MHC class II-restricted T cells) responding to the same antigen, OVA. The results show that 4-1BBL plays an important role in the in vivo recall responses of both CD4 + and CD8 + T cells.…”

Section: Introductionmentioning

confidence: 99%

Expression and function of 4‐1BB during CD4 versus CD8 T cell responses in vivo

Dawicki

Watts

2004

Eur J Immunol

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4-1BBL -/-mice have a defect in recall CD8 + T cell responses to viruses, whereas CD4 + T cell responses to virus are unimpaired in these mice. In contrast, both CD4 + and CD8 + T cells respond to 4-1BB ligand (4-1BBL) in vitro. To clarify the role of 4-1BB/4-1BBL in CD4 + versus CD8 + T cell responses in vivo, we compared CD4 (OT-II) and CD8 (OT-I) TCR transgenic T cells responding to the same antigen in an in vivo adoptive transfer model in 4-1BBL +/+ versus 4-1BBL -/-mice. During primary and secondary responses, expression of 4-1BB on in vivo-activated TCR transgenic T cells was earlier and more transient than previously observed in vitro, correlating with expression of the early activation antigen CD69 and preceding the transition to the CD44 hi state. Although 4-1BB is expressed early in the primary response, there was no effect of 4-1BBL deficiency on initial CD8 T cell expansion and only a minor effect on initial CD4 T cell expansion. The major effect of 4-1BB/4-1BBL interaction is on the T cell recall response. This is due to effects of 4-1BBL on maintenance of T cell numbers at the end of the primary response with additional effects of 4-1BBL on secondary expansion of T cells.

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“…1,7 No difference in the levels of serum IL-10 between WT and Bim À / À mice was observed at several time points (unpublished data). To determine whether the effects of Bim on subset differentiation were T-cell intrinsic, we adoptively transferred small 20 and infected with LCMV a day later (Figure 2a). Subsequent analysis of blood revealed that host and donor p14 cells equally contributed to the response on day 10, indicating that they did not suppress the endogenous response (Figure 2b).…”

mentioning

confidence: 99%

Bim controls IL-15 availability and limits engagement of multiple BH3-only proteins

Kurtuluş

Sholl

et al. 2014

Cell Death Differ

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During the effector CD8 þ T-cell response, transcriptional differentiation programs are engaged that promote effector T cells with varying memory potential. Although these differentiation programs have been used to explain which cells die as effectors and which cells survive and become memory cells, it is unclear if the lack of cell death enhances memory. Here, we investigated effector CD8 þ T-cell fate in mice whose death program has been largely disabled because of the loss of Bim. Interestingly, the absence of Bim resulted in a significant enhancement of effector CD8 þ T cells with more memory potential. Bim-driven control of memory T-cell development required T-cell-specific, but not dendritic cell-specific, expression of Bim. Both total and T-cell-specific loss of Bim promoted skewing toward memory precursors, by enhancing the survival of memory precursors, and limiting the availability of IL-15. Decreased IL-15 availability in Bim-deficient mice facilitated the elimination of cells with less memory potential via the additional pro-apoptotic molecules Noxa and Puma. Combined, these data show that Bim controls memory development by limiting the survival of pre-memory effector cells. Further, by preventing the consumption of IL-15, Bim limits the role of Noxa and Puma in causing the death of effector cells with less memory potential.

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Visualization of peptide-specific T cell immunity and peripheral tolerance induction in vivo

Cited by 899 publications

References 38 publications

Differences in maintenance of CD8⁺ and CD4⁺ bacteria‐specific effector‐memory T cell populations

Differences in maintenance of CD8⁺ and CD4⁺ bacteria‐specific effector‐memory T cell populations

Expression and function of 4‐1BB during CD4 versus CD8 T cell responses in vivo

Bim controls IL-15 availability and limits engagement of multiple BH3-only proteins

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Visualization of peptide-specific T cell immunity and peripheral tolerance induction in vivo

Cited by 899 publications

References 38 publications

Differences in maintenance of CD8+ and CD4+ bacteria‐specific effector‐memory T cell populations

Differences in maintenance of CD8+ and CD4+ bacteria‐specific effector‐memory T cell populations

Expression and function of 4‐1BB during CD4 versus CD8 T cell responses in vivo

Bim controls IL-15 availability and limits engagement of multiple BH3-only proteins

Contact Info

Product

Resources

About

Differences in maintenance of CD8⁺ and CD4⁺ bacteria‐specific effector‐memory T cell populations

Differences in maintenance of CD8⁺ and CD4⁺ bacteria‐specific effector‐memory T cell populations