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CD4 + CD25 + CD62 + T‐Regulatory Cell Subset Has Optimal Suppressive and Proliferative Potential
Author(s) -
Fu Shuang,
Yopp Adam C.,
Mao Xia,
Chen Dongmei,
Zhang Nan,
Chen Dan,
Mao Minwei,
Ding Yaozhong,
Bromberg Jonathan S.
Publication year - 2004
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1046/j.1600-6143.2003.00293.x
Subject(s) - il 2 receptor , foxp3 , immunology , population , regulatory t cell , medicine , transplantation , l selectin , t cell , immune system , cell adhesion molecule , environmental health
CD4 + CD25 + regulatory T cells (Treg) are potent suppressors, and play important roles in autoimmunity and transplantation. Recent reports suggest that CD4 + CD25 + Treg are not a homogeneous cell population, but the differences in phenotype, function, and mechanisms among different subsets are unknown. Here, we demonstrate CD4 + CD25 + Treg cells can be divided into subsets according to cell‐surface expression of CD62L. While both subsets express foxp3 and are anergic, the CD62L + population is more potent on a per cell basis, and proliferates and maintains suppressive function far better than the CD62L– population and unseparated CD4 + CD25 + Treg. The CD62L + population preferentially migrates to CCL19, MCP‐1 and FTY720. Both CD62L + and CD62L– subsets prevent the development of autoimmune gastritis and colitis induced by CD4 + CD25–CD45RB high cells in severe combined immunodeficiency (SCID) mice. Overall, these results suggest CD4 + CD25 + Treg are not a homogenous cell population, but can be divided into at least two subsets according to CD62L expression. The CD62L + subset is a more potent suppressor than the CD62L– population or unfractionated CD4 + CD25 + Treg cells, can be expanded far more easily in culture, and is more responsive to chemokine‐driven migration to secondary lymphoid organs. These properties may have significant implications for the clinical manipulation of the CD4 + CD25 + CD62L + cells.