期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 194, 期 5, 页码 601-614出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.194.5.601
关键词
fucosyltransferase; selectin; T lymphocyte; Th1; Tc1
资金
- NCI NIH HHS [1 P01 CA71932] Funding Source: Medline
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 deficient 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. These defects are not accounted for by alterations in the number or function of 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 deficiencies, respectively, in the complement of naive T lymphocytes available in lymph nodes for antigen-dependent activation, expansion, differentiation, and dissemination. Fuc-TVII deficiency also deletes expression of E- and P-selectin ligands by Th1 and T cytotoxic 1 (Tc1) lymphocytes, annuls T cell 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 and Fuc-TVII to L-selectin ligand synthesis, and to lymphocyte recruitment, are requisite components of the primary cellular immune response, and assign an essential role to Fuc-TVII in control of E- and P-selectin ligand expression by Th1 and Tc1 lymphocytes.
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