Decreased accessory cell function by human monocytic cells after infection with HIV.
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.
Petit
A J
AJ
Central Laboratory, Netherlands Red Cross Blood Transfusion Service, Amsterdam.
Tersmette
M
M
Terpstra
F G
FG
de Goede
R E
RE
van Lier
R A
RA
Miedema
F
F
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
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