Successful adoptive T-cell immunotherapy of solid tumors will require improved expansion and cytotoxicity of tumor-directed T cells within tumors. Providing recombinant or transgenic cytokines may produce the desired benefits but is associated with significant toxicities， constraining clinical use. To circumvent this limitation， we constructed a constitutively signaling cytokine receptor， C7R， which potently triggers the IL7 signaling axis but is unresponsive to extracellular cytokine. This strategy augments modified T-cell function following antigen exposure， but avoids stimulating bystander lymphocytes. Coexpressing the C7R with a tumor-directed chimeric antigen receptor (CAR) increased T-cell proliferation， survival， and antitumor activity during repeated exposure to tumor cells， without T-cell dysfunction or autonomous T-cell growth. Furthermore， C7R-coexpressing CAR T cells were active against metastatic neuroblastoma and orthotopic glioblastoma xenograft models even at cell doses that had been ineffective without C7R support. C7R may thus be able to enhance antigen-specific T-cell therapies against cancer. The constitutively signaling C7R system developed here delivers potent IL7 stimulation to CAR T cells， increasing their persistence and antitumor activity against multiple preclinical tumor models， supporting its clinical development. .