Antigen presentation in HIV infection

Knight, Stella C.; Macatonia, Steven E.; Patterson, Steven

doi:10.1007/978-94-011-2980-0_3

Cited by 2 publications

(1 citation statement)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SIGNALING TO CD4 + T CELLS Occasional reports in the literature describe defects in antigen presentation, and this has been proposed as a major factor in reduction in T cell numbers and function (39,65,(80)(81)(82)(83)(84)(85). Early experiments showed that low density cells separated from peripheral blood of HIV-infected patients contain low numbers of MHC class II-expressing cells and reduced capacity to stimulate primary allogeneic T cell proliferation (75).…”

Section: Changed Signaling To Lymphocytes By DCmentioning

confidence: 99%

Bone Marrow–derived Dendritic Cells, Infection With Human Immunodeficiency Virus, and Immunopathology

Knight

Patterson

1997

Annu. Rev. Immunol.

116

View full text Add to dashboard Cite

Dendritic cells (DC) exposed to HIV-1 show nonproductive infection that may become productive as they mature. The distribution of DC within genital mucosa and their susceptibility to infection particularly with clade E viruses could be reflected in the ease of heterosexual transmission. Carriage of virus and viral antigen by DC into lymph nodes may allow clustering and activation of T cells and production of protective immune responses. However, secondary infection of activated T cells from infected DC could cause dissemination of virus and loss of infected DC and T cells. In asymptomatic infection, fewer dendritic cells with reduced capacity to stimulate CD4 T cell proliferation are found before evidence of T cell abnormalities, and these early changes in antigen-presenting cells may result in a decline in the production of CD4 memory T cells. However, DC fuel ongoing production of antibody to HIV-1. Signaling by DC to T cells may thus underlie two major features of early HIV infection--loss in CD4+ memory T cells and persistence of antibody production. In AIDS, infected dendritic and epithelial cells within the thymus may affect maturation and contribute to loss of the "naive" T cell population. Further loss of memory T cells may occur through syncytium formation with infected DC. Finally, in AIDS patients, there is a failure in the development and the function of DC from CD34+ stem cells. In conclusion, the infection of dendritic cells, loss in their numbers, and changed signaling to T cells may shape the pattern of immunity during infection with HIV-1. Conversely, treatments that reverse the defect in antigen presentation by DC may improve cell-mediated immunity.

show abstract