Journal
IMMUNOLOGIC RESEARCH
Volume 42, Issue 1-3, Pages 166-181Publisher
HUMANA PRESS INC
DOI: 10.1007/s12026-008-8057-6
Keywords
Lentiviral vector; CD28; PD-1; TCR; Chimeric immunoreceptor; Zinc-finger nuclease; NOG mice; Immunotherapy; Adoptive T cell therapy
Categories
Funding
- NCI NIH HHS [R41 CA130547-01, P01 CA066726, P01 CA066726-110006, R41 CA130547-02, R01 CA113783, R01 CA113783-03, R01 CA113783-04, R41 CA130547] Funding Source: Medline
- NHLBI NIH HHS [T32 HL007775] Funding Source: Medline
- NIAID NIH HHS [U19 AI066290-010003, P01 AI080192, K08 AI073102-02, R01 AI057838-04, U19 AI066290-030003, U19 AI066290-040003, P01 AI080192-010003, R01 AI057838-05, R21 AI060477-02, R01 AI057838, R01 AI057838-03, R21 AI060477, U19 AI066290-020003, R01 AI057838-01A1, R01 AI057838-02, U19 AI066290, K08 AI073102, R21 AI060477-01A1] Funding Source: Medline
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To be effective for the treatment of cancer and infectious diseases, T cell adoptive immunotherapy requires large numbers of cells with abundant proliferative reserves and intact effector functions. We are achieving these goals using a gene therapy strategy wherein the desired characteristics are introduced into a starting cell population, primarily by high efficiency lentiviral vector-mediated transduction. Modified cells are then expanded using ex vivo expansion protocols designed to minimally alter the desired cellular phenotype. In this article, we focus on strategies to (1) dissect the signals controlling T cell proliferation; (2) render CD4 T cells resistant to HIV-1 infection; and (3) redirect CD8 T cell antigen specificity.
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