Fuc-TVII is required for T helper 1 and T cytotoxic 1 lymphocyte selectin ligand expression and recruitment in inflammation, and together with Fuc-TIV regulates naive T cell trafficking to lymph nodes

To determine hose the alpha (1,3)fucosyltransferases Fuc-TIV and Fuc-TVII, and the selectin ligands they control may contribute to the adaptive immune response, contact hypersensitivity (CHS) leas characterized in mice defici ent in either or both enzymes. We find a substantial CHS deficiency in Fuc- TVII-/- mice, and a complete deficiency in Fuc-TIV-/-/Fuc-TVII-/- mice. The se defects are not accounted for by alterations in the number or function o f epidermal Langerhans cells required fur cutaneous antigen processing and presentation. By contrast, defective CHS in Fuc-TVII-/- mice or Fuc-TIV-/-/ Fuc-TVII-/- mice is attributed in part to prominent, or nearly complete def iciencies, respectively, in the complement of naive T lymphocytes available in lymph nodes for antigen-dependent activation, expansion, differentiatio n, and dissemination. Fuc-TVII deficiency also deletes expression of E- and P-selectin ligands by Th1 and T cytotoxic 1 (Tc1) lymphocytes, annuls T ce ll trafficking to inflamed cutaneous sites in vivo, and thereby controls an essential component of the efferent phase of the cutaneous immune response . These observations indicate that collaborative contributions of Fuc-TIV a nd Fuc-TVII to L-selectin ligand synthesis, and to lymphocyte recruitment, are requisite components of the primary cellular immune response, and assig n an essential role to Fuc-TVII in control of E- and P-selectin ligand expr ession by Th1 and Tc1 lymphocytes.