Submitted to: Journal of Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/18/1997
Publication Date: N/A
Citation: Interpretive Summary: Resistance or susceptibility to an infection by a parasite is determined by the interaction between the parasite and the immune system of the host that it infects. Knowledge of which outcome, resistance or susceptibility, will occur, and how it is regulated by the host, is important in the design of effective strategies to control infectious diseases of humans and livestock. The current study demonstrates that worm parasites stimulate a strong and characteristic response that leads to effective immunity when cells that bear particular cell surface molecules are activated. A specific pattern of molecular interactions is required in order for the complete set of host immune responses to be effectively activated. This information is relevant to researchers that are interested in producing vaccines against worm parasites for the control of the level and intensity of the infection. This observation is unique because it shows for the first time that worms induce a pattern of cell surface molecular interaction that is not the same as that required by isolated proteins that are often used to immunize against the parasite. This observation suggests that new stimulators of the immune system must accompany vaccination with isolated proteins if the response is to be effective against the worm infection. Thus, as novel subunit vaccines are planned their ability to stimulate a complete protective immune response must be determined.
Technical Abstract: Blocking B7 ligand costimulatory molecules can inhibit a primary T dependent immune response, but whether these interactions also mediate ongoing or memory immune responses is less clear. Development of immunotherapies based on blocking B7 ligand interactions would be limited if they were effective only at the initiation of an immune response. This commentary discusses the conditions under which T helper effector and memory cells may or may not require B7 ligand interactions for their function.