Human immunodeficiency virus type 1 evades T-helper responses by exploiting antibodies that suppress antigen processing |
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Authors: | Chien Peter C Cohen Sandra Tuen Michael Arthos James Chen Pei-de Patel Sukeshi Hioe Catarina E |
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Institution: | Department of Pathology, New York University School of Medicine and Veterans Affairs, New York Harbor Healthcare System, New York, NY 10010, USA. |
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Abstract: | T-helper responses are important for controlling chronic viral infections, yet T-helper responses specific to human immunodeficiency virus type 1 (HIV-1), particularly to envelope glycoproteins, are lacking in the vast majority of HIV-infected individuals. It was previously shown that the presence of antibodies to the CD4-binding domain (CD4bd) of HIV-1 glycoprotein 120 (gp120) prevents T-helper responses to gp120, but their suppressive mechanisms were undefined (C. E. Hioe et al., J. Virol. 75:10950-10957, 2001). The present study demonstrates that gp120, when complexed to anti-CD4bd antibodies, becomes more resistant to proteolysis by lysosomal enzymes from antigen-presenting cells such that peptide epitopes are not released and presented efficiently by major histocompatibility complex class II molecules to gp120-specific CD4 T cells. Antibodies to other gp120 regions do not confer this effect. Thus, HIV may evade anti-viral T-helper responses by inducing and exploiting antibodies that conceal the virus envelope antigens from T cells. |
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