Costimulation of CD8 T cell responses by OX40.

Abstract	The persistence of functional CD8 T cell responses is dependent on checkpoints established during priming. Although naive CD8 cells can proliferate with a short period of stimulation, CD4 help, inflammation, and/or high peptide affinity are necessary for the survival of CTL and for effective priming. Using OX40-deficient CD8 cells specific for a defined Ag, and agonist and antagonist OX40 reagents, we show that OX40/OX40 ligand interactions can determine the extent of expansion of CD8 T cells during responses to conventional protein Ag and can provide sufficient signals to confer CTL-mediated protection against tumor growth. OX40 signaling primarily functions to maintain CTL survival during the initial rounds of cell division after Ag encounter. Thus, OX40 is one of the costimulatory molecules that can contribute signals to regulate the accumulation of Ag-reactive CD8 cells during immune responses.
Authors	Pratima Bansal-Pakala, Beth S Halteman, Mary Huey-Yu Cheng, Michael Croft
Journal	Journal of immunology (Baltimore, Md. : 1950) (J Immunol) Vol. 172 Issue 8 Pg. 4821-5 (Apr 15 2004) ISSN: 0022-1767 [Print] United States
PMID	15067059 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References	Membrane Glycoproteins OX40 Ligand Receptors, OX40 Receptors, Tumor Necrosis Factor Tnfrsf4 protein, mouse Tnfsf4 protein, mouse Tumor Necrosis Factors
Topics	Adoptive Transfer Animals CD8-Positive T-Lymphocytes (immunology, metabolism, transplantation) Cell Aggregation (immunology) Cell Division (genetics, immunology) Cell Survival (genetics, immunology) Cytotoxicity, Immunologic (genetics) Immunity, Cellular (genetics) Lymphocyte Activation (genetics, immunology) Lymphopenia (genetics, immunology) Membrane Glycoproteins (metabolism, physiology) Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic OX40 Ligand Peritoneal Neoplasms (genetics, immunology, pathology) Receptors, OX40 Receptors, Tumor Necrosis Factor (deficiency, genetics, metabolism, physiology) Signal Transduction (immunology) T-Lymphocytes, Regulatory (cytology, immunology) Tumor Necrosis Factors

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.

Realize the full power of the drug-disease research graph!