Intestinal homeostasis is maintained by a hierarchy of immune defences acting in concert to minimize contact between luminal microorganisms and the intestinal epithelial cell surface. The intestinal mucus layer, covering the gastrointestinal (GI) tract epithelial cells, contributes to mucosal homeostasis by limiting bacterial invasion. In this study, we used T-cell-deficient (TCR^-/-) mice to examine whether and how T-cells modulate the properties of the intestinal mucus layer. Increased susceptibility of TCR^-/- mice to dextran sodium sulphate (DSS)-induced colitis is associated with a reduced number of goblet cells. Alterations in the number of goblet cells and crypt lengths were observed in the small intestine (SI) and colon of TCR^-/- mice compared to C57BL/6 wt mice. Addition of keratinocyte growth factor (KGF) to small intestinal organoid cultures from TCR^-/- mice showed a marked increase in crypt growth, and both goblet cell number and redistribution along the crypts. There was no apparent difference in the thickness or organisation of the mucus layer between TCR^-/- and wt mice, as measured in vivo. However, T-cell deficiency led to reduced sialylated mucins in association with increased gene expression of gel-secreting Muc2 and membrane-bound mucins, including Muc13 and Muc17. Collectively, these data provide evidence that T cells play an important role in maintenance of mucosal homeostasis by regulating mucin expression and promoting goblet cell function in the small intestine.