Impaired signalling in T cells from patients with colorectal cancer in response to IL-2 and IL-7. — Australasian Cytometry Society
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Impaired signalling in T cells from patients with colorectal cancer in response to IL-2 and IL-7. (24035)

Shirley Shen 1 , Edward Taylor 1 , Kirsten Ward-Hartstonge 1 , John McCall 2 , Fran Munro 2 , Roslyn Kemp 1
  1. Department of Microbiology and Immunology, Otago School of Medical Sciences, University of Otago, Dunedin, New Zealand
  2. Department of Surgical Sciences, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand

T cells are key components of the anti-tumour response, particularly in mediating an effector function against colorectal cancer (CRC) to prevent tumour progression. The survival and proliferation of T cells are dependent on signals from IL-2 and IL-7; these cytokines are therefore important for initiating and maintaining an immune response against colorectal tumours.

The aim of this study was to measure the phosphorylation of signalling molecules downstream of IL-2 and IL-7 stimulation in T cells isolated from patients with CRC. This was achieved by using phosphoflow cytometry to measure STAT5 phosphorylation in T cells isolated from PBMCs or primary tumour tissue. We hypothesised that patients with CRC would have a dysregulation in T cell signalling in response to IL-2 and IL-7 when compared to healthy subjects.

We have shown that T cells from PBMCs isolated from CRC patients have more STAT5 phosphorylation after IL-7 stimulation than T cells from healthy control PBMCs; however, this increase was not due to an increased expression of IL-7Rα, nor was it a function of age. Preliminary data show that there may also be aberrant signalling in response to IL-2 and IL-7 in T cells from tumour tissue compared to non-tumour bowel tissue from the same patients. Results from this study will contribute to understanding the functionality of tumour-infiltrating T cells in patients with CRC, which can potentially aid in the development of new immunotherapies to target T cell responses in CRC.

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