Limited Density of an Antigen Presented by RMA-S Cells Requires B7-1/CD28 Signaling to Enhance T-Cell Immunity at the Effector Phase |
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Authors: | Xiao-Lin Li Marjolein Sluijter Elien M Doorduijn Shubha P Kale Harris McFerrin Yong-Yu Liu Yan Li Madhusoodanan Mottamal Xin Yao Fengkun Du Baihan Gu Kim Hoang Yen H Nguyen Nichelle Taylor Chelsea R Stephens Thorbald van Hall Qian-Jin Zhang |
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Institution: | 1. Department of Biology, Xavier University of Louisiana, New Orleans, Louisiana, United States of America.; 2. Clinical Oncology, K1-P, Leiden University Medical Center, Leiden, the Netherlands.; 3. Department of Basic Pharmaceutical Sciences, University of Louisiana at Monroe, Monroe, Louisiana, United States of America.; 4. College of Chemistry & Environmental Science, Hebei University, Hebei Province, Baoding, China.; Ohio State University, United States of America, |
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Abstract: | The association of B7-1/CD28 between antigen presenting cells (APCs) and T-cells provides a second signal to proliferate and activate T-cell immunity at the induction phase. Many reports indicate that tumor cells transfected with B7-1 induced augmented antitumor immunity at the induction phase by mimicking APC function; however, the function of B7-1 on antitumor immunity at the effector phase is unknown. Here, we report direct evidence of enhanced T-cell antitumor immunity at the effector phase by the B7-1 molecule. Our experiments in vivo and in vitro indicated that reactivity of antigen-specific monoclonal and polyclonal T-cell effectors against a Lass5 epitope presented by RMA-S cells is increased when the cells expressed B7-1. Use of either anti-B7-1 or anti-CD28 antibodies to block the B7-1/CD28 association reduced reactivity of the T effectors against B7-1 positive RMA-S cells. Transfection of Lass5 cDNA into or pulse of Lass5 peptide onto B7-1 positive RMA-S cells overcomes the requirement of the B7-1/CD28 signal for T effector response. To our knowledge, the data offers, for the first time, strong evidence that supports the requirement of B7-1/CD28 secondary signal at the effector phase of antitumor T-cell immunity being dependent on the density of an antigenic peptide. |
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