Toward cellular-based therapies for HIV infection.
Infection with HIV-1 progressively erodes immune function, leading ultimately to multiple hematopoietic cytopenias. In advanced HIV disease, anemia, neutropenia, and thrombocytopenia occur in a large fraction of patients and are reflective of a striking inability of the bone marrow to accomplish a compensatory increase in production. No failure of compensatory production is greater than that of the T lymphoid system, where despite apparently effective control of HIV replication, restoration of anti-HIV immunity does not occur. Recent technical developments have provided considerable insight into hematopoietic dysfunction in HIV disease and, in particular, in vivo T cell generation. This article will review some of the mechanisms participating in immune regeneration, the stakes involved in effectively accomplishing full reconstitution, and potential approaches to enhance the limited endogenous regenerative process.
Scadden
David T
DT
Partners AIDS Research Center and MGH Cancer Center, Massachusetts General Hospital, Harvard Medical School, Boston 02129, USA. scadden.david@mgh.harvard.edu
D019380:Anti-HIV Agents / Q000627:therapeutic use*; D017690:Cell Transplantation; D015658:HIV Infections / Q000628:therapy*; D006801:Humans; D013234:Stem Cells / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D013950:Thymus Gland / Q000473:pathology
D019380:Anti-HIV Agents