Table 5.
Methods of GVHD prophylaxis and therapy.
| I. Methods of GVHD prophylaxis |
|---|
| a. Pharmacotherapy |
| • Calcineurin inhibitor (Tacrolimus∧, Cyclosporin A*) |
| • Inhibitors of cell proliferation (Mycophenolate Mofetil, Methotrexate*∧, PT-Cyclophosphamide) |
| • Corticosteroids |
| • mTOR inhibitors (e.g., Sirolimus, Everolimus) |
| b. Depletion of donor T-lymphocytes |
| •In vivo (Anti-T-lymphocyte globulin~, Alemtuzumab) |
| •Ex vivo (CD34+ selection, CD3+ TCRαβ/CD19 depletion, CD3+ TCRαβ/CD19 depletion with iCasp9 suicide gene TCRαβ add-back, CD3+ CD45RA+ depletion) |
| II. GVHD Therapies |
| a. Corticosteroids |
| b. Immunosuppressive agents |
| c. Cytokine-receptor agonists |
| • Anti-interleukin-2R |
| • Anti-interleukin-6R |
| • Anti-TNFR |
| d. Extracorporeal photopheresis |
| • 8-Methoxypsor-alen (8-MOP) + UVA radiation |
| e. Mesenchymal stromal cells |
| III. New potential approaches under investigation |
| • PI3K inhibitors |
| • JAK inhibitors |
| • MEK inhibitors |
| • Aurora A inhibitors |
| • ROCK-1 inhibitors |
| • CDK2 inhibitors |
*
In Combination, Europe gold standard.
∧
In Combination, America gold standard.
~
In Combination. GVHD, graft versus host disease; PT, Post-Transplant; TCR, T Cell Receptor; TNFR, Tumor Necrosis Factor Receptor; PI3K, Phosphoinositide 3-kinase; JAK, Janus kinase; MEK, mitogen-activated protein kinase kinase; ROCK-1, Rho-associated kinase 1; CDK2, Cyclin-dependent kinase 2.