TY - JOUR
T1 - Monocyte accessory cell function in patients infected with the human immunodeficiency virus
AU - Twigg, Homer L.
AU - Weissler, Jonathan C.
AU - Yoffe, Boris
AU - Ball, Edward J.
AU - Lipscomb, Mary F.
N1 - Funding Information:
’ Supported by Grants Al-21951, HL-01797, and MO1 RR-00633 from the National Institutes of Health. ’ To whom reprint requests should be addressed at Division of Pulmonary and Critical Care, Indiana University Medical Center, 1001 West 10th St., OPW 425. Indianapolis, IN 46202. 3 Recipient of an ALAiATS Research Training Fellowship award. 4 Currently on faculty in the Division of Pulmonary and Critical Care Medicine, Indiana University School of Medicine. Indianapolis, Indiana. ’ Current address: Department of Internal Medicine, Baylor College of Medicine, Houston, Texas. ’ Current address: Community Blood Center, Dayton Regional Tissue Bank, Dayton. Ohio.
PY - 1991/6
Y1 - 1991/6
N2 - Previous studies suggested that peripheral blood monocytes (Mo) from HIV-infected patients were poor accessory cells (AC), although most of these studies were limited by using autologous T cells as responders. Using allogeneic T cells from uninfected volunteers as responders, the current studies demonstrate that Mo from infected individuals were comparable to Mo from uninfected volunteers as AC in Con A and pokeweed mitogen-stimulated lymphocyte proliferation assays, but were inferior to normal Mo in stimulating a mixed leukocyte reaction. This deficiency was not explained by HIV Mo-induced suppression of lymphoproliferation or by death of responding CD4 lymphocytes induced by HIV transmission from infected Mo in 6-day MLR cultures. Mo from HIV-infected patients retained the ability to stimulate mumps-specific T cell lines in response to antigen, demonstrating that Mo from these individuals could process and display antigen on their cell surface in association with a functional DR molecule. Taken together these results suggest that Mo from HIV-infected patients (i) retain the ability to act as AC in T cell responses to mitogenic signals or to stimulate already activated antigen-specific T cells, but (ii) fail to stimulate resting and/or unprimed T cells in response to alloantigen and perhaps de novo antigen exposure. It is possible this Mo defect may have an adverse effect on the immune responsiveness of HIV-infected individuals.
AB - Previous studies suggested that peripheral blood monocytes (Mo) from HIV-infected patients were poor accessory cells (AC), although most of these studies were limited by using autologous T cells as responders. Using allogeneic T cells from uninfected volunteers as responders, the current studies demonstrate that Mo from infected individuals were comparable to Mo from uninfected volunteers as AC in Con A and pokeweed mitogen-stimulated lymphocyte proliferation assays, but were inferior to normal Mo in stimulating a mixed leukocyte reaction. This deficiency was not explained by HIV Mo-induced suppression of lymphoproliferation or by death of responding CD4 lymphocytes induced by HIV transmission from infected Mo in 6-day MLR cultures. Mo from HIV-infected patients retained the ability to stimulate mumps-specific T cell lines in response to antigen, demonstrating that Mo from these individuals could process and display antigen on their cell surface in association with a functional DR molecule. Taken together these results suggest that Mo from HIV-infected patients (i) retain the ability to act as AC in T cell responses to mitogenic signals or to stimulate already activated antigen-specific T cells, but (ii) fail to stimulate resting and/or unprimed T cells in response to alloantigen and perhaps de novo antigen exposure. It is possible this Mo defect may have an adverse effect on the immune responsiveness of HIV-infected individuals.
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U2 - 10.1016/0090-1229(91)90039-D
DO - 10.1016/0090-1229(91)90039-D
M3 - Article
C2 - 1827620
AN - SCOPUS:0025727827
SN - 0090-1229
VL - 59
SP - 436
EP - 448
JO - Clinical Immunology and Immunopathology
JF - Clinical Immunology and Immunopathology
IS - 3
ER -