Effect of HIV on antigen presentation by dendritic cells and macrophages |
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| Affiliation: | 1. Department of Ophthalmology, Weill Cornell Medical College, New York, New York;2. Retina Associates of Orange County, Laguna Hills, California;3. Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York, New York;4. Allogeneic Bone Marrow Transplantation Service, Memorial Sloan-Kettering Cancer Center, New York, New York;5. Miami Cancer Institute, Miami, Florida;6. Department of Ophthalmology, Illinois Eye & Ear Infirmary, University of Illinois-Chicago, Chicago, Illinois;7. Department of Ophthalmology & Vision Science, University of California Davis Eye Center, Sacramento, California;8. Department of Ophthalmology, Wilmer Eye Institute of Johns Hopkins University, Baltimore, Maryland;3. Department of Orthopedics, Southwest Hospital, Third Military Medical University, Chongqing 400038, China;4. Department of Biomedical Materials Science, Southwest Hospital, Third Military Medical University, Chongqing 400038, China;5. Department of Blood Purification, General Hospital of Shenyang Military Area Command, Shenyang 110000, China;1. Department of Medical Laboratory Sciences, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria;2. The Brainwill Laboratory, Osogbo, Osun State, Nigeria;3. Reproductive Biology and Toxicology Research Laboratory, Oasis of Grace Hospital, Osogbo, Osun State, Nigeria;4. Department of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria;5. Department of Morbid Anatomy, Obafemi Awolowo University Teaching Hospital Complex (OAUTHC), Ile Ife, Osun State, Nigeria;6. Department of Physiology, University of Ilorin, Ilorin, Kwara State, Nigeria |
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| Abstract: | The antigen-presenting function of dendritic cells (DC) and macrophages (MO) following infection with HIV in vitro was examined. Using non-infected cells, DC, but not MO, stimulated primary proliferative responses in allogeneic lymphocytes in the mixed leukocyte reaction. Both DC and MO stimulated secondary responses to influenza virus and to tetanus toxoid in autologous T lymphocytes. After exposure of DC and MO to HIV1 in vitro for 2 days, 27 % of DC but < 1 % MO became infected as assessed by in situ hybridization. DC were blocked in their capacity to stimulate responses to alloantigens or to the recall antigens. By contrast, MO retained the ability to stimulate responses to the recall antigens. Similar effects during in vivo infection would allow activated T-cell clones to respond to antigens presented by MO early in infection. However, any loss of activated T cells might prove cumulative and damaging in the absence of an effective DC recruitment mechanism for resting T cells. |
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