IntroductionDendritic cells (DCs) are professional antigen-presenting cells that can induce optimal activation of naive T lymphocytes. They have developed unique cross-presentation pathways allowing major histocompatibility complex (MHC) class I-restricted presentation of antigens of exogenous origin, taken up by endocytosis or phagocytosis. Cross-presentation is crucial for the stimulation of CD8 ϩ T lymphocytes and therefore induction of immunity and tolerance to antigens that are not directly synthesized in the cytosol of DCs, such as antigens from other tissues, from tumors or from pathogens that do not infect DCs predominantly. [1][2][3][4][5] DCs are required for cross-presentation in vivo. 6 So understanding the mechanism of cross-presentation by DCs is an important issue to provide optimized immune therapies.DCs participate in the phagocytic clearance of apoptotic debris, from which they cross-present antigens, 7 a phenomenon observed in vivo. 8,9 Apoptosis was thought to be tolerogenic, whereas necrosis was truly immunogenic through the release of nuclear or cytosolic molecules that serve as endogenous adjuvants. 10,11 Indeed, cross-tolerization of tissue-restricted Ag is enhanced when proapoptotic stimuli are included, and conversely, is prevented by expression of an antiapoptotic molecule. 12 Moreover, a DC-specific deficiency in uptake of apoptotic material inhibits cross-tolerization in vivo. 13 However, cross-presentation from apoptotic cells can lead to immunogenicity in the presence of proinflammatory signals, CD4 help, 14,15 infection, 16 through the surface expression of ER molecules, such as calreticulin, or through the release of HMGB1 by apoptotic cells. 17 The focus in the past years has been on the mechanism of cell death leading to cross-presentation. The current concept of "death-defying immunity" is fascinating and must have physiologic relevance. 15,18 But is death necessary to induce cross-presentation?We have shown that cross-presentation of HIV antigens from apoptotic infected CD4 ϩ T lymphocytes, which are the main targets of viral replication, is a very efficient process in vitro. Surprisingly, transfer and cross-presentation of HIV antigens from live infected CD4 ϩ T lymphocytes by human monocyte-derived DCs were found to be as efficient as cross-presentation from apoptotic cells. 19 This novel mechanism of cross-presentation is currently not fully characterized but needs cell-to-cell contact, similarly to the "nibbling" process described previously that gave rise to tumor antigen cross-presentation. 20,21 Although crosspresentation from live cells led to efficient restimulation of memory HIV-specific CD8 ϩ T lymphocytes from HIV-infected patients, 19 it is still unknown whether this mechanism could apply to naive T lymphocytes in vivo. Cross-presentation of antigens from live cells has never been taken into account, although live cells may be a major source of antigen in vivo. It was important to establish whether this new cross-presentation mechanism was only an artifact found ...

As previously reported, a C-type retrovirus, referred to as retrovirus X was isolated from HIV infected cells. In order to further characterize this virus, the proviral DNA was cloned and sequenced. The organization of the genome (8379 bp) appeared to be typical of the mammalian type C retroviruses. The virus was shown to be closely related to the gibbon ape leukaemia virus (GALV) with 87% similarity when the sequence was compared with the published genome of the Seato strain of GALV. At the level of the long terminal repeat where comparison was possible with other strains, the closest relationship was found with the San Francisco strain of GALV and with the simian sarcoma virus. These results suggest that the isolate should be considered as a strain of GALV.