Inflammation within the tracheal lumen (asterisks) after allogeneic tracheal transplantation is decreased in the absence of the leukotriene receptor BLT1 (right).

T cell recruitment to sites of inflammation has traditionally been thought to depend primarily on the interaction between chemotactic peptides (chemokines), produced by cells in the inflamed tissue, and their corresponding receptors on T cells. However, chemotactic lipid mediators such as leukotrienes and prostaglandins—known for attracting neutrophils and eosinophils—have recently been shown to contribute to T cell recruitment. Early lung invasion by T cells in response to an inhaled allergen was blunted in mice lacking the leukotriene B4 (LTB4) receptor BLT1. But this decrease did not persist, calling into question the significance of leukotriene-induced T cell migration in disease.

Medoff and colleagues now show that BLT1-deficient mice were less likely to develop T cell-mediated airway obstruction following allogeneic tracheal transplantation, demonstrating that leukotriene-induced T cell migration contributes to disease. This finding is consistent with previous studies showing that inhibition of BLT1 signaling was protective in other mouse models of allogeneic transplantation. However the contribution of T cell trafficking was never evaluated in those models.

Elimination of BLT1 did not completely reverse T cell infiltration into the lung, suggesting that LTB4 does not act alone. The authors suggest that chemokines may also contribute to the T cell recruitment—a possibility they are currently investigating.