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The Journal of Immunology, 2004, 173: 866-873.
Copyright © 2004 by The American Association of Immunologists

Antigen-Specific Lymphocyte Sequestration in Lymphoid Organs: Lack of Essential Roles for {alpha}L and {alpha}4 Integrin-Dependent Adhesion or G{alpha}i Protein-Coupled Receptor Signaling1

Carrie N. Arnold2, Eugene C. Butcher and Daniel J. Campbell3

Department of Pathology, Laboratory of Immunology and Vascular Biology, Stanford University School of Medicine, Stanford, CA 94305 and Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA 94304

Selective lymphocyte sequestration was described over 30 years ago as the transient withdrawal of Ag-specific lymphocytes from the circulation as a result of their activation in secondary lymphoid organs. We used a TCR-transgenic adoptive transfer system to further characterize the Ag and adjuvant dependence of this process in mice. In addition, we examined the contribution of the {alpha}L and {alpha}4 integrin chains as well as G{alpha}i protein-coupled receptor signaling to the retention of Ag-specific T cells in peripheral lymph nodes. Our results demonstrate that selective lymphocyte sequestration is T cell autonomous and adjuvant independent, and that the duration of sequestration is not controlled by the continued presence of Ag in secondary lymphoid organs. This process is not critically dependent on the {alpha}L and {alpha}4 integrin chains or G{alpha}i protein-coupled receptor signaling. Selective lymphocyte sequestration may be mediated by redundant mechanisms and/or controlled by novel or nonclassical adhesion or trafficking molecules.




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