Scientific Articulation during Collaborative Digital Game-Based Learning Enhances Learning of Immunology.

Digital game-based learning has been used to help learners grasp complex concepts in science subjects such as immunology. The aim of this study was to examine whether playing a digital game collaboratively would encourage articulation of scientific terminology and concepts, and whether this would result in learning gains. Forty-seven students at a tertiary institution (17-19 y of age) played a game (n = 22) or watched a video of the game (n = 25) in small groups. This was followed by an activity to document the key learning points. Pretest and posttest results showed that although both groups had learning gains, the game-based learning group outperformed the video group for gains in procedural knowledge, suggesting that playing the game helped students to better internalize the steps involved in the immune response. For the game-based learning group, there was a positive correlation between the number of scientific terms articulated and the gains in the test scores. However, for the video group, there was no correlation. The implications for designing digital game-based learning activities for learning are discussed. The study was carried out in an online environment due to the COVID-19 pandemic mandating home-based learning at the time. The discussion also focuses on how the findings can be applied in an online and face-to-face context.

STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation.

T helper (TH)-cell subsets, such as TH1 and TH17, mediate inflammation in both peripheral tissues and central nervous system. Here we show that STAT5 is required for T helper-cell pathogenicity in autoimmune neuroinflammation but not in experimental colitis. Although STAT5 promotes regulatory T cell generation and immune suppression, loss of STAT5 in CD4+ T cells resulted in diminished development of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Our results showed that loss of encephalitogenic activity of STAT5-deficient autoreactive CD4+ T cells was independent of IFN-γ or interleukin 17 (IL-17) production, but was due to the impaired expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), a crucial mediator of T-cell pathogenicity. We further showed that IL-7-activated STAT5 promotes the generation of GM-CSF-producing CD4+ T cells, which were preferentially able to induce more severe EAE than TH17 or TH1 cells. Consistent with GM-CSF-producing cells being a distinct subset of TH cells, the differentiation program of these cells was distinct from that of TH17 or TH1 cells. We further found that IL-3 was secreted in a similar pattern as GM-CSF in this subset of TH cells. In conclusion, the IL-7-STAT5 axis promotes the generation of GM-CSF/IL-3-producing TH cells. These cells display a distinct transcriptional profile and may represent a novel subset of T helper cells which we designate as TH-GM.