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SHP-1 in T cells limits the production of CD8 effector cells without impacting the formation of long-lived central memory cells. | LitMetric

AI Article Synopsis

  • Naive CD8 T lymphocytes expand during viral and cancer responses, creating both short-lived effector cells and potential long-term memory cells (memory precursor effector cells).
  • The activation of these T cells is influenced by signals they receive, including antigenic, costimulatory, and cytokine signals, which determine the type of CD8 populations formed.
  • Research using conditional knockout mice lacking the phosphatase SHP-1 in T cells revealed that SHP-1 affects different CD8 T cell subpopulations, limiting short-lived effector cell production while leaving the memory precursor cell pool intact.

Article Abstract

During responses against viruses and malignancies, naive CD8 T lymphocytes expand to form both short-lived effector cells and a population containing cells with the potential to be long-lived and participate in memory responses (memory precursor effector cells). The strength of antigenic, costimulatory, and cytokine signals during responses impacts the magnitude and type of CD8 populations formed. In vitro studies have revealed that the tyrosine phosphatase Src homology region 2 domain-containing phosphatase-1 (SHP-1) regulates signal transduction from receptors on T cells including the TCR, helping set the activation threshold, and therefore may shape responses of mature CD8 T cells in vivo. Analysis of CD8 T cells from motheaten mice, which are globally deficient in SHP-1, proved problematic due to cell-extrinsic effects of SHP-1 deficiency in non-T cells on CD8 T cells. Therefore, a conditional knockout of SHP-1 in mature single-positive T cells was developed to analyze cell-intrinsic consequences of complete and partial SHP-1 deficiency on CD8 T cell responses to acute viral infection. The results demonstrated that SHP-1 has disparate effects on subpopulations of responding cells, limiting the magnitude and quality of primary and secondary responses by reducing the number of short-lived effector cells generated without affecting the size of the memory precursor effector cell pool that leads to formation of long-term memory.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2980864PMC
http://dx.doi.org/10.4049/jimmunol.1001362DOI Listing

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