Fig. 1.

Gut microbiota mediates the differentiation of naïve T-cells either into pro-inflammatory Th17 or anti-inflammatory, Tregs. These effector T-cells then migrate to systemic circulation from mLN. Th17 boosts effector T-cells, mainly mediated via IL-17, whereas Tregs suppress effector T-cell function, mediated via IL-10. Specific gut taxa may potentially be harnessed to enhance CAR T-cell responses in several ways (figure’s left to right): By influencing pre-CAR conditioning; by using specific, narrow-spectrum antibiotics to deplete select, detrimental gut microbes; suppression of Foxp3+ Tregs and hence circumventing Treg-induced CAR T-cell suppression; upregulation of IL-6/STAT3 signature; direct activation of CAR T-cells (similar mechanism as that of endogenous T-cells)