Antigen–specific release of β-chemokines by anti-HIV-1 cytotoxic T lymphocytes

[1]  R. Phillips,et al.  Antagonism of cytotoxic T lymphocyte‐mediated lysis by natural HIV‐1 altered peptide ligands requires simultaneous presentation of agonist and antagonist peptides , 1997, European journal of immunology.

[2]  Nancy Sullivan,et al.  CCR5 Levels and Expression Pattern Correlate with Infectability by Macrophage-tropic HIV-1, In Vitro , 1997, The Journal of experimental medicine.

[3]  R P Johnson,et al.  Suppression of human immunodeficiency virus type 1 replication by CD8+ cells: evidence for HLA class I-restricted triggering of cytolytic and noncytolytic mechanisms , 1997, Journal of virology.

[4]  P. Klenerman,et al.  Positive selection of HIV-1 cytotoxic T lymphocyte escape variants during primary infection. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[5]  Xiping Wei,et al.  Antiviral pressure exerted by HIV-l-specific cytotoxic T lymphocytes (CTLs) during primary infection demonstrated by rapid selection of CTL escape virus , 1997, Nature Medicine.

[6]  Martin A. Nowak,et al.  Late escape from an immunodominant cytotoxic T-lymphocyte response associated with progression to AIDS , 1997, Nature Medicine.

[7]  A. Fauci,et al.  CD8+ T-cell-derived soluble factor(s), but not β-chemokines RANTES, MIP-1α, and MIP-1β, suppress HIV-1 replication in monocyte/macrophages , 1996 .

[8]  Anthony S. Fauci,et al.  Host factors and the pathogenesis of HIV-induced disease , 1996, Nature.

[9]  V. Harden,et al.  Chemokines and HIV–1 second receptors , 1996, Nature Medicine.

[10]  D. Weissman,et al.  HIV replication in CD4+ T cells of HIV-infected individuals is regulated by a balance between the viral suppressive effects of endogenous beta-chemokines and the viral inductive effects of other endogenous cytokines. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[11]  F. Buseyne,et al.  Dual function of a human immunodeficiency virus (HIV)-specific cytotoxic T-lymphocyte clone: inhibition of HIV replication by noncytolytic mechanisms and lysis of HIV-infected CD4+ cells. , 1996, Virology.

[12]  C. Walker,et al.  RANTES, MIP-1α and MIP-1β are not involved in the inhibition of HIV-1SF33 replication mediated by CD8+ T-cell clones , 1996 .

[13]  M. Bukrinsky,et al.  Chemokines and HIV replication , 1996, Nature.

[14]  J. Levy,et al.  Controlling HIV pathogenesis: the role of the noncytotoxic anti-HIV response of CD8+ T cells. , 1996, Immunology today.

[15]  A. Lanzavecchia,et al.  Different responses are elicited in cytotoxic T lymphocytes by different levels of T cell receptor occupancy , 1996, The Journal of experimental medicine.

[16]  D. Taub,et al.  β Chemokines costimulate lymphocyte cytolysis, proliferation, and lymphokine production , 1996, Journal of leukocyte biology.

[17]  S. Arya,et al.  Identification of RANTES, MIP-1α, and MIP-1β as the Major HIV-Suppressive Factors Produced by CD8+ T Cells , 1995, Science.

[18]  M. Barnardo,et al.  Phototyping: comprehensive DNA typing for HLA-A, B, C, DRB1, DRB3, DRB4, DRB5 & DQB1 by PCR with 144 primer mixes utilizing sequence-specific primers (PCR-SSP). , 1995, Tissue antigens.

[19]  J. Sheridan,et al.  Requirement of MIP-1 alpha for an inflammatory response to viral infection. , 1995, Science.

[20]  D. Taub,et al.  CD8+ and CD45RA+ human peripheral blood lymphocytes are potent sources of macrophage inflammatory protein 1α, interleukin‐8 and RANTES , 1995, European journal of immunology.

[21]  B. Dewald,et al.  Interleukin-8 and related chemotactic cytokines--CXC and CC chemokines. , 1994, Advances in immunology.

[22]  S. Rowland-Jones,et al.  An antigen processing polymorphism revealed by HLA‐B8‐restricted cytotoxic T lymphocytes which does not correlate with TAP gene polymorphism , 1993, European Journal of Immunology.

[23]  D. Goeddel,et al.  Human macrophage inflammatory protein alpha (MIP-1 alpha) and MIP-1 beta chemokines attract distinct populations of lymphocytes , 1993, The Journal of experimental medicine.

[24]  B. Walker,et al.  Human immunodeficiency virus type 1-specific cytotoxic T lymphocytes release gamma interferon, tumor necrosis factor alpha (TNF-alpha), and TNF-beta when they encounter their target antigens , 1993, Journal of virology.

[25]  S. Burrows,et al.  Peptide epitope induced apoptosis of human cytotoxic T lymphocytes. Implications for peripheral T cell deletion and peptide vaccination. , 1993, Journal of immunology.

[26]  D. Richman,et al.  Human immunodeficiency virus type 1 mutants resistant to nonnucleoside inhibitors of reverse transcriptase arise in tissue culture. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[27]  Charles R. M. Bangham,et al.  Human immunodeficiency virus genetic variation that can escape cytotoxic T cell recognition , 1991, Nature.

[28]  E A Emini,et al.  Viral resistance to human immunodeficiency virus type 1-specific pyridinone reverse transcriptase inhibitors , 1991, Journal of virology.

[29]  D. Nixon,et al.  HIV-1 gag-specific cytotoxic T lymphocytes defined with recombinant vaccinia virus and synthetic peptides , 1988, Nature.