Document 0099
 DOCN  M94A0099
 TI    Modulation of antigen-presenting capacity of human monocytes by HIV-1
       GP120 molecule fragments.
 DT    9412
 AU    Zembala M; Pryjma J; Plucienniczak A; Szczepanek A; Ruggiero I; Jasinski
       M; Colizzi V; Department of Clinical Immunology, Jagiellonian
       University; Medical College, Cracow, Poland.
 SO    Immunol Invest. 1994 Apr;23(3):189-99. Unique Identifier : AIDSLINE
       MED/94350405
 AB    The two fragments of HIV-1 gp120 molecule were synthesized to study
       their interaction with human monocytes. Previous observations indicated
       that recombinant gp120 fragment (aa residues 410-511) encompassing CD4
       binding region (rp120cd) induced tumour necrosis factor alpha (TNF)
       production in monocytes, while a similar fragment (rp120) not containing
       the CD4 binding sequence (aa 446-511) was inactive. This paper shows
       that rp120cd depressed monocyte ability to present antigen (PPD) to
       autologous T lymphocytes while rp120 was noninhibitory. The rp120cd
       interacted with monocytes but not T lymphocytes. Anti-TNF receptor type
       A antibody (utr-1) prevented the depression of antigen presentation
       caused by rp120cd, which suggested a role for TNF and its receptor. The
       depression of antigen presentation was seen only when monocytes were
       treated with rp120cd before, but not after, pulse with antigen. Parallel
       changes were observed in PPD-induced IL-6 production. Thus, induction of
       TNF by gp120 may be associated with impairment of antigen-presenting
       capacity of monocytes seen in AIDS patients.
 DE    Antigen Presentation  Cells, Cultured  Human  HIV Envelope Protein
       gp120/*IMMUNOLOGY  Interleukin-6/BIOSYNTHESIS  Monocytes/*IMMUNOLOGY
       Peptide Fragments/CHEMICAL SYNTHESIS/IMMUNOLOGY  Receptors, Tumor
       Necrosis Factor/IMMUNOLOGY  Support, Non-U.S. Gov't
       T-Lymphocytes/IMMUNOLOGY  Tuberculin/IMMUNOLOGY  Tumor Necrosis
       Factor/BIOSYNTHESIS  JOURNAL ARTICLE

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