The pandemic has brought challenges to teaching lab and research skills. Here Nigel Francis and colleagues explore the diverse approaches taken to replace lab‐based immunology teaching, explain how networks of educators have driven this innovation and discuss the importance of retaining best practice into the future.

Chemokine-directed leukocyte migration is essential for immune and inflammatory responses. The chemokine receptor CCR7, by responding to chemokines CCL19 and CCL21, is critical in regulating the recruitment of dendritic cells (DC), from peripheral tissues to draining lymph nodes (LNs). CCR7 is required for DC entry into lymphatic vessels, and for the passage of these cells across subcapsular sinus of the lymph node. Here, they initiate adaptive immune responses by priming antigen-specific T cells. CCRL1, an unexpected second receptor for CCL19 and CCL21, belongs to the family of atypical chemokine receptors and is able to bind and sequester extracellular chemokine without exhibiting any form of classical chemokine signaling. CCRL1 function in vivo is still unclear. We have generated CCRL1 deficient mice but find no perturbations in DC numbers in the LNs at rest, and DC trafficking from the skin is normal after painting with hapten (FITC). However, if FITC is applied after the induction of cutaneous inflammation, FITC+ DCs fail to reach draining LNs. Using a combination of microscopy and flow cytometry, we show that DCs are unable to enter lymphatic vessels and remain trapped in the skin. These data will be presented in the context of new insights into the identity of CCRL1-expressing cells in the skin and lymph node. Collectively, our data indicate that CCRL1-mediated regulation of CCL19 and/or CCL21 is required to maintain DC departure from the skin during inflammation.

PDAC is predicted to become the second commonest cause of cancer death in the western world by 2030. Aggressive invasion and early metastases are characteristic of the disease, and even the few patients eligible for potentially curative resection inevitably develop recurrent or metastatic disease. We now show that CXCR2 signalling is upregulated in human pancreatic cancer, predominantly in neutrophils at the tumour invasive edge. In mouse models, genetic ablation or inhibition of CXCR2 abrogated metastasis while inhibition also slowed tumorigenesis, particularly when combined with chemotherapy. Depletion of neutrophils also suppressed metastasis, suggesting a key role for CXCR2 in establishing and maintaining the metastatic niche. Indications from trials thus far suggest that immunotherapy will not work as a single agent strategy in pancreatic cancer patients. Importantly, we find that loss or inhibition of CXCR2 improved T-cell entry and combined inhibition of CXCR2 and PD1 in mice with established disease caused a significant extension of survival. Thus, our data highlight two novel therapeutic opportunities for PDAC: first the use of CXCR2 inhibitors in surgically-resected patients to prevent recurrence at distant sites, and second, the use of CXCR2 inhibition in combination with immunotherapy in surgically unresectable advanced disease. This abstract is also being presented as Poster B55 Citation Format: Colin Steele, Saadia Karim, Josh Leach, Peter Bailey, Andrew Biankin, Rob Nibbs, Simon Barry, Owen Sansom, Jen Morton.{Authors}. CXCR2 Inhibition Suppresses Metastasis and Improves the Response to Immunotherapy in Pancreatic Cancer. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; 2016 May 12-15; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(24 Suppl):Abstract nr PR10.