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In additional embodiments, stimulation of the T cells comprises contacting the T cells with an anti-CD28 antibody or a CD28-binding fragment thereof, B7-1 or a CD28-binding fragment thereof, or B7-2 or a CD28-binding fragment thereof. 4. The method of claim 1, wherein stimulation of the T cells comprises contacting the T cells with an anti-CD28 antibody or a CD28-binding fragment thereof, B7-1 or a CD28-binding fragment thereof, or B7-2 or a CD28-binding fragment thereof. 9. The method of claim 8, wherein the extracellular domain comprises an antibody or antigen binding fragment that binds the antigen. 3. The method of claim 1, wherein activation of the T cells comprises contacting the T cells with an anti-CD3 antibody or CD3-binding fragment thereof. In additional embodiments, the inhibitor of the PI3K/AKT/mTOR pathway inhibits HSP activation of AKT. In particular embodiments, the inhibitor of the PI3K/AKT/mTOR pathway inhibits mTORC2 activation of AKT. In certain embodiments, the inhibitor of the PI3K/AKT/mTOR pathway inhibits DNA-PK activation of AKT.

However, most, if not all adoptive immunotherapy strategies require T cell activation and expansion steps to generate a clinically effective, therapeutic dose of T cells. In addition, existing T cell activation/expansion methods are normally coupled with substantial T cell differentiation and usually result in short-lived effects, including short-lived survival and a lack of persistence and lack of in vivo expansion of the transferred T cells. For example, T cell expansion often requires labor intensive and expensive cloning, and/or multiple rounds of activation/expansion to achieve therapeutically relevant T cell numbers. To date, clinical efficacy of engineered T cell adoptive immunotherapies is limited by poor T cell expansion and persistence after infusion into patients. The invention generally provides adoptive T cell immunotherapies comprising persistent and potent anti-tumor T cell compositions and methods of making the same. 12. The method of claim 8, further comprising a hinge region polypeptide. 13. The method of claim 12, wherein the hinge region polypeptide comprises a hinge region of IgG1 or CD8.alpha.. In particular embodiments, the CAR comprises a signal peptide.

15. The method of claim 14, wherein the signal peptide comprises an IgG1 heavy chain signal polypeptide or a CD8.alpha. In additional embodiments, the CAR comprises a signal peptide. In particular embodiments, the hinge region polypeptide comprises a hinge region of IgG1 or CD8.alpha.. In further embodiments, the hinge region polypeptide comprises a hinge region of IgG1 or CD8.alpha.. 2. The method of claim 1, wherein the method comprises isolating peripheral blood mononuclear cells as the source of T cells. In particular embodiments, the methods contemplated herein comprise isolating peripheral blood mononuclear cells as the source of T cells. In certain embodiments, the cells comprise a CAR. In other particular embodiments, the cells comprise a viral vector encoding an engineered TCR or CAR. In some embodiments, the cells are transduced with the viral vector prior to T cell proliferation. In certain embodiments, the cells are transduced with the viral vector after T cell proliferation.

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