title: Polymorphonuclear neutrophils in Wegener's granulomatosis acquire characteristics of antigen presenting cells.
abstract: BACKGROUND
  Constitutive expression of major histocompatibility complex (MHC) class II antigens and of the co-stimulatory receptors CD80 and CD86 is restricted to professional antigen presenting cells. Polymorphonuclear neutrophils (PMN) of healthy donors are negative for those antigens. Our recent study, however, found that PMN of patients with active Wegener's granulomatosis acquired MHC class II antigens.
  
  
  METHODS
  To continue and extend the previous study results, PMN and monocytes of 60 patients with Wegener's granulomatosis, 24 patients with microscopic polyangiitis (MPA), 20 patients with acute bacterial infection, and 53 healthy donors were analyzed for the expression of MHC class II antigens as well as of CD80 and CD86. Moreover, induction on PMN of MHC class II expression was studied, as was antigen presentation as a possible functional consequence.
  
  
  RESULTS
  PMN of patients with acute, active Wegener's granulomatosis expressed MHC class II antigens, CD80 and CD86; on monocytes up-regulation of MHC class II was seen. In contrast, PMN of patients with inactive disease, or with relapse, patients with microscopic polyangiitis or with bacterial infections expressed neither MHC class II, nor CD80 or CD86. PMN of healthy donors acquired these antigens when cultured in the presence of T cells or T cell-derived cytokines. The PMN were then able to present to T cell antigens in a MHC-class II restricted manner.
  
  
  CONCLUSIONS
  During active disease, the PMN of patients with Wegener's granulomatosis acquire characteristics of antigen presenting cells, whereas the PMN of patients with MPA or bacterial infection do not. The finding reflects differences in the pattern of the respective inflammatory response and suggests new effector functions of PMN. Moreover, MHC class II expression on PMN could serve as a novel marker for active Wegener's granulomatosis.
authors.affiliation: Institut für Immunologie und Medizinische Klinik, Universität Heidelberg, Heidelberg, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Iking-Konert
authors.forename: S
authors.initials: S
authors.lastname: Vogt
authors.forename: M
authors.initials: M
authors.lastname: Radsak
authors.forename: C
authors.initials: C
authors.lastname: Wagner
authors.forename: G M
authors.initials: GM
authors.lastname: Hänsch
authors.forename: K
authors.initials: K
authors.lastname: Andrassy
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000938:Antigen-Presenting Cells / Q000276:immunology*; D015703:Antigens, CD / Q000032:analysis; D018122:B7-1 Antigen / Q000032:analysis; D051940:B7-2 Antigen; D001424:Bacterial Infections / Q000276:immunology; D005260:Female; D014890:Granulomatosis with Polyangiitis / Q000276:immunology*; D000949:Histocompatibility Antigens Class II / Q000032:analysis*; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology*; D012016:Reference Values; D014657:Vasculitis / Q000276:immunology
chemical_list: D015703:Antigens, CD; D018122:B7-1 Antigen; D051940:B7-2 Antigen; C497964:CD86 protein, human; D000949:Histocompatibility Antigens Class II; D008562:Membrane Glycoproteins