Infusion Of Cytomegalovirus Specific Cytotoxic T Lymphocytes From A Sero-Negative Donor Can Facilitate Resolution Of Infection And Immune Reconstitution
Department of Pediatrics, Blood and Marrow Transplant Program, University of California, San Francisco, CA. The Pediatric Infectious Disease Journal
(Impact Factor: 2.72).
12/2008; 28(1):65-7. DOI: 10.1097/INF.0b013e318182026f
We report a stem cell transplant patient with a therapy-refractory cytomegalovirus (CMV) infection who received CMV-specific T cells from his sero-negative stem cell donor. This donor received the Towne strain CMV vaccine, and T cells were expanded using monocytes pulsed with pp65 overlapping peptides. CMV DNA decreased after the CTL infusion, and CMV-specific cytotoxicity increased. This strategy could be implemented in similar situations or with persistent viremia post-transplant.
Available from: sciencedirect.com
Value in Health 05/2005; 8(3):387-387. DOI:10.1016/S1098-3015(10)63044-6 · 3.28 Impact Factor
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ABSTRACT: Impairment of cellular immunity upon hematopoietic stem cell transplantation (HSCT) may lead to serious clinical manifestations induced by human cytomegalovirus (HCMV) and varicella-zoster virus (VZV) infections. Although the clinical presentations, preferential organ involvement and clinical courses are different, infections with both herpesviruses are similar with respect to many pathophysiological aspects and the therapeutic strategies that are employed to combat them. Antiviral drug prophylaxis and therapy are successfully used to limit the risk of reactivated HCMV and VZV infections, but are unable to absolutely prevent episodes of virus disease in long-term follow-up after HSCT. Control of infection requires the re-establishment of protective antiviral cellular immunity in the host. Here we review the most recent developments in the field of HCMV and VZV immunotherapy with specific emphasis on the question of how vaccines against HCMV and VZV may aid in enhancing the reconstitution of antiviral immunity after HSCT, and thereby support the control of these two agents by transplant recipients.
Expert Review of Vaccines 09/2009; 8(8):999-1021. DOI:10.1586/erv.09.58 · 4.21 Impact Factor
Available from: ncbi.nlm.nih.gov
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ABSTRACT: Inherited defects in components of the nonhomologous end-joining DNA repair mechanism produce a T-B-NK+ severe combined immunodeficiency disease (SCID) characterized by heightened sensitivity to ionizing radiation. Patients with the radiosensitive form of SCID may also have increased short- and long-term sensitivity to the alkylator-based chemotherapy regimens that are traditionally used for conditioning before allogeneic hematopoietic cell transplantation (HCT). Known causes of radiosensitive SCID include deficiencies of Artemis, DNA ligase IV, DNA-dependent protein kinase catalytic subunit, and Cernunnos-XLF, all of which have been treated with HCT. Because of these patients' sensitivity to certain forms of chemotherapy, the approach to donor selection and the type of conditioning regimen used for a patient with radiosensitive SCID requires careful consideration. Significantly more research needs to be done to determine the long-term outcomes of patients with radiosensitive SCID after HCT and to discover novel nontoxic approaches to HCT that might benefit those patients with intrinsic radiosensitivity and chemosensitivity as well as potentially all patients undergoing an HCT.
Immunology and allergy clinics of North America 02/2010; 30(1):125-42. DOI:10.1016/j.iac.2009.10.004 · 1.82 Impact Factor
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