TY - JOUR
T1 - Neutrophils from patients with advanced human immunodeficiency virus infection have impaired complement receptor function and preserved Fcγ receptor function
AU - Monari, Claudia
AU - Casadevall, Arturo
AU - Pietrella, Donatella
AU - Bistoni, Francesco
AU - Vecchiarelli, Anna
PY - 1999
Y1 - 1999
N2 - Interleukin (IL)-8 production by human polymorphonuclear leukocytes (PMNL) to Cryptococcus neoformans is related to complement activation. Generation of the bioactive fragments C3a and C5a is responsible for IL-8 release. IL-8 production was analyzed in response to C. neoformans by PMNL from persons with early- and late-stage (>400 and <200 CD4 cells/mm3, respectively) human immunodeficiency virus (HIV) infection who were at high risk for cryptococcosis. IL-8 release by PMNL from persons with early-stage infection and from healthy donors was similar; however, PMNL from persons with late-stage HIV infection had significantly impaired IL-8 production, which correlated with reduced IL-8 response to C3a and C5a proteins and decreased CD88 expression. Addition of murine monoclonal antibody (MAb) 18B7 promoted phagocytosis and restored IL-8 release consistent with integrity of FcγRIII. These results provide evidence for a selective defect in CD88 expression on PMNL from persons with late-stage HIV infection. However, Fcγ receptor expression in PMNL appears to be intact and allows MAb to glucuronoxylomannan to positively influence PMNL function.
AB - Interleukin (IL)-8 production by human polymorphonuclear leukocytes (PMNL) to Cryptococcus neoformans is related to complement activation. Generation of the bioactive fragments C3a and C5a is responsible for IL-8 release. IL-8 production was analyzed in response to C. neoformans by PMNL from persons with early- and late-stage (>400 and <200 CD4 cells/mm3, respectively) human immunodeficiency virus (HIV) infection who were at high risk for cryptococcosis. IL-8 release by PMNL from persons with early-stage infection and from healthy donors was similar; however, PMNL from persons with late-stage HIV infection had significantly impaired IL-8 production, which correlated with reduced IL-8 response to C3a and C5a proteins and decreased CD88 expression. Addition of murine monoclonal antibody (MAb) 18B7 promoted phagocytosis and restored IL-8 release consistent with integrity of FcγRIII. These results provide evidence for a selective defect in CD88 expression on PMNL from persons with late-stage HIV infection. However, Fcγ receptor expression in PMNL appears to be intact and allows MAb to glucuronoxylomannan to positively influence PMNL function.
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U2 - 10.1086/315099
DO - 10.1086/315099
M3 - Article
C2 - 10515814
AN - SCOPUS:0032729808
SN - 0022-1899
VL - 180
SP - 1542
EP - 1549
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 5
ER -