title: Decreased accessory cell function by human monocytic cells after infection with HIV.
abstract: We studied the effect of HIV infection on the human monocytic cell line U937. The cell line was infected with cellfree HIV, strain HTLV-IIIB. After 3 wk, a high reverse transcriptase activity was continuously detected in the supernatant of the cell line. Neither cytopathic effects nor changes in cell growth were observed. After infection, accessory cell function on T cell proliferation induced by anti-CD3 mAb of both IgG1 and IgG2a subclasses and Con A was tested. Accessory cell function provided by U937 cells started to decline 3 wk after inoculation with HIV. This correlated with detectable reverse transcriptase activity. The remaining accessory cell capacity varied between 10 and 60% of accessory cell function mediated by noninfected U937 cells. It was excluded that decreased FcR expression on U937/HIV cells contributed to the accessory cell defect in the anti-CD3-driven system. IL-2R expression on T cells, cocultivated with U937/HIV and anti-CD3, was minimal. The accessory cell defect could only be partly overcome by addition of rIL-2 or IL-1. Addition of high titer (10(4) TCID50) HIV or U937/HIV cells did not affect T cell proliferation, which rules out that the observed inhibition is caused by HIV infection of T cells or suppressive effects of U937/HIV cells. These results suggest that infection of APC may contribute to the induction of immunologic abnormalities in early HIV infection. Thus, monocytes/macrophages may not only serve as a reservoir for the dissemination of HIV, but may be an important target cell through which the immune system is affected.
authors.affiliation: Central Laboratory, Netherlands Red Cross Blood Transfusion Service, Amsterdam.
authors.forename: A J
authors.initials: AJ
authors.lastname: Petit
authors.forename: M
authors.initials: M
authors.lastname: Tersmette
authors.forename: F G
authors.initials: FG
authors.lastname: Terpstra
authors.forename: R E
authors.initials: RE
authors.lastname: de Goede
authors.forename: R A
authors.initials: RA
authors.lastname: van Lier
authors.forename: F
authors.initials: F
authors.lastname: Miedema
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D000938:Antigen-Presenting Cells / Q000276:immunology*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology; D002460:Cell Line; D006801:Humans; D007106:Immune Sera / Q000494:pharmacology; D007165:Immunosuppression Therapy; D007375:Interleukin-1 / Q000494:pharmacology; D007376:Interleukin-2 / Q000378:metabolism / Q000494:pharmacology; D008213:Lymphocyte Activation; D009000:Monocytes / Q000276:immunology* / Q000382:microbiology; D011961:Receptors, Fc / Q000032:analysis; D017452:Receptors, IgG; D011971:Receptors, Immunologic / Q000096:biosynthesis; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D007106:Immune Sera; D007375:Interleukin-1; D007376:Interleukin-2; D011961:Receptors, Fc; D017452:Receptors, IgG; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D011994:Recombinant Proteins