title: Blood-borne signals that induce anterior chamber-associated immune deviation after intracameral injection of antigen.
abstract: OBJECTIVE
  Anterior chamber-associated immune deviation (ACAID) is elicited by an antigen-specific signal that escapes the antigen-containing eye and travels through the blood to the spleen. Two types of ACAID-inducing signals have been described: those associated with blood-borne monocytes, and a soluble factor found in serum. The authors sought to understand the basis for the existence of two distinct types of ACAID-inducing signals.
  
  
  METHODS
  Different kinds of antigens (soluble, cell associated, particulate) were injected into the anterior chamber (AC) of normal, presensitized, and immunodeficient mice. In addition, peritoneal exudate cells were pulsed in vitro with different kinds of antigen in the presence of transforming growth factor beta and then evaluated for the ability to induce ACAID in naive (nonsensitized) as well as T- and B-cell-deficient recipients.
  
  
  RESULTS
  Among antigens injected into the AC, inert particulate antigens could not induce ACAID, but soluble and cell-associated (minor histocompatibility) antigens generated cell-associated ACAID-inducing signals. In contrast, antigens injected into the AC of presensitized mice generated ACAID-inducing signals that were soluble and located in the plasma fraction of blood. All ACAID-inducing signals created in vitro with soluble, particulate, or cell-associated antigens induced ACAID in vivo.
  
  
  CONCLUSIONS
  Cell-associated ACAID-inducing signals are generated in naive mice regardless of the kind of antigen, and these signals arise from mobile intraocular antigen-presenting cells. However, when antigen is injected into the AC of presensitized mice, a soluble signal emerges, perhaps derived from T cells that enter the antigen-containing eye. Together, these signals dictate that subsequent exposures to ocular antigen will not evoke immunogenic inflammation.
authors.affiliation: Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts 02114, USA.
authors.forename: J W
authors.initials: JW
authors.lastname: Streilein
authors.forename: S
authors.initials: S
authors.lastname: Okamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Hara
authors.forename: M
authors.initials: M
authors.lastname: Kosiewicz
authors.forename: B
authors.initials: B
authors.lastname: Ksander
mesh_terms: D000818:Animals; D000867:Anterior Chamber / Q000276:immunology*; D000941:Antigens / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D001769:Blood / Q000276:immunology*; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D007267:Injections; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D015778:Minor Histocompatibility Antigens / Q000276:immunology; D009161:Mycobacterium / Q000276:immunology; D010529:Peritoneal Cavity / Q000166:cytology; D012710:Serum Albumin, Bovine / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D014407:Tumor Cells, Cultured / Q000276:immunology
chemical_list: D000941:Antigens; D015778:Minor Histocompatibility Antigens; D012710:Serum Albumin, Bovine