| Abstract: |
CD4, a T cell receptor for major histocompatibility complex class II antigen, is a key regulator of immunological reactivities. When engaged together with the T cell antigen receptor, CD4 enhances immune reactions, whereas when ligated independently of the antigen receptor CD4 inhibits the activation of T cells or initiates their deletion. CD4 serves also as a receptor for the human immunodeficiency virus (HIV), which binds the receptor with high avidity through its envelope molecule, gp120. Studies in tissue culture have shown that its affinity to CD4 gives the virus opportunities to utilize CD4‐mediated signaling and to manipulate immunocytes. We show here in human CD4 transgenic mice that appropriately cross‐linked HIV envelope protein causes massive deletion of HIV‐reactive T cells in vivo. Copyright © 1994 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim |
| Keywords: |
signal transduction; controlled study; nonhuman; flow cytometry; t lymphocyte; animal cell; mouse; animal; mice; cell death; cells, cultured; spleen; animal experiment; virus receptor; immunoregulation; mice, transgenic; t lymphocyte receptor; lymphocyte activation; antibodies, monoclonal; major histocompatibility antigen class 2; cd4-positive t-lymphocytes; transgene; antibody specificity; human immunodeficiency virus; acquired immune deficiency syndrome; cd4 antigen; protein cross linking; hiv-1; virus protein; deletion; hiv antibodies; hiv envelope protein gp120; envelope protein; cd4; gp120; glycoprotein gp 120; human; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.
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