title: Expression of complement receptors and regulatory proteins on alveolar CD4+ lymphocytes from human immunodeficiency virus-1 infected individuals.
abstract: Several lines of evidence suggest a dysregulation of the complement system in human immunodeficiency virus-1 (HIV-1) infected patients. The aim of this study was to elucidate whether CD4+ alveolar lymphocytes from HIV-1 infected patients show a loss of complement regulatory proteins that would render these cells susceptible to antibody-dependent complement-mediated cytotoxicity. We investigated the expression of complement regulatory (CD46, CD55, CD59) and complement receptor (CR1, CR2, CR3, CR4) proteins on alveolar cells by flow cytometry. Cells were obtained by bronchoalveolar lavage from 17 HIV-1 infected and 12 HIV-1 negative individuals. Expression of adhesion molecules (leucocyte functional associated antigen-1 (LFA-1), intercellular adhesion molecule-1 (ICAM-1)) and CD30 were evaluated in patient subgroups. In addition, interleukin (IL)-1beta, tumour necrosis factor alpha (TNF-alpha), IL-4 and interferon gamma (IFN-gamma) concentrations were measured in supernatants of alveolar cells. We found a significantly reduced expression of CD46 and CD59 on CD4+ alveolar lymphocytes from HIV-1 infected individuals, whereas the expression of CR3, CR4, ICAM-1 and CD30 was increased. IL-1beta and TNF-alpha concentration in supernatants of alveolar cells was augmented in HIV-1 infected patients, but did not correlate with the expression of surface molecules. IFN-gamma concentration was also increased and showed an inverse relationship to the surface expression of CD30 on CD4+. Our data suggest that in human immunodeficiency virus-1 infection an increased level of activation is associated with a diminished expression of complement regulatory proteins on CD4+ alveolar lymphocytes. This phenomenon might contribute to the depletion of CD4+ lymphocytes and the local immunodeficiency in the pulmonary compartment.
authors.affiliation: Dept Internal Medicine II, Medical University Lübeck, Germany.
authors.forename: S P
authors.initials: SP
authors.lastname: Aries
authors.forename: B
authors.initials: B
authors.lastname: Schaaf
authors.forename: F
authors.initials: F
authors.lastname: Hansen
authors.forename: K
authors.initials: K
authors.lastname: Weyrich
authors.forename: V
authors.initials: V
authors.lastname: Kurowski
authors.forename: R
authors.initials: R
authors.lastname: Dennin
authors.forename: K
authors.initials: K
authors.lastname: Dalhoff
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism / Q000502:physiology*; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism*; D003167:Complement Activation; D003165:Complement System Proteins / Q000502:physiology*; D016207:Cytokines / Q000378:metabolism; D005260:Female; D015658:HIV Infections / Q000378:metabolism* / Q000473:pathology; D015497:HIV-1; D006801:Humans; D008297:Male; D008875:Middle Aged; D011650:Pulmonary Alveoli / Q000378:metabolism* / Q000473:pathology; D011951:Receptors, Complement / Q000378:metabolism*
chemical_list: D015703:Antigens, CD; D016207:Cytokines; D011951:Receptors, Complement; D003165:Complement System Proteins