May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
ACAID Dependence on an Intact Peripheral Sympathetic Nervous System and Immunizing Antigen Dose
Author Affiliations & Notes
  • X. Li
    Pathology, UConn Health Center, Farmington, CT, United States
  • S. Taylor
    Pathology, UConn Health Center, Farmington, CT, United States
  • B. Wohlfert
    Pathology, UConn Health Center, Farmington, CT, United States
  • Y. Wang
    Pathology, UConn Health Center, Farmington, CT, United States
  • J. O' Rourke
    Pathology, UConn Health Center, Farmington, CT, United States
  • R.E. Cone
    Pathology, UConn Health Center, Farmington, CT, United States
  • Footnotes
    Commercial Relationships  X. Li, None; S. Taylor, None; B. Wohlfert, None; Y. Wang, None; J. O' Rourke, None; R.E. Cone, None.
  • Footnotes
    Support  EY13243
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 749. doi:
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      X. Li, S. Taylor, B. Wohlfert, Y. Wang, J. O' Rourke, R.E. Cone; ACAID Dependence on an Intact Peripheral Sympathetic Nervous System and Immunizing Antigen Dose . Invest. Ophthalmol. Vis. Sci. 2003;44(13):749.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Recently, we reported that antigen-specific NK thymocytes, (AC-Thyreg) are induced by dendritic cells that appear in the blood following the intracameral injection of antigen. In turn, AC-Thyreg activate immunoregulatory T cells (AC-SPL) in the spleens of immunized recipients. This study examines two new aspects of the induction of ACAID: (i) influence of a recipients immunizing antigen dose on the generation of ACAID or AC-SPL induced by transferred AC-Thyreg,( ii) the influence of the sympathetic nervous system (SNS), which densely inervates the uvea, thymus and spleen, on the induction of ACAID. Methods: AC-Thyregwere obtained from Balb/c mice receiving intracameral TNP-BSA. AC-SPL were obtained from TNP-BSA-immunized mice one week following i.v. AC-Thyreg or intracameral injection of antigen. Mice were chemically sympathetomized two days before systemic immunization by the ip injection of 6-hyroxydopamine (6-OHDA) which destroys peripheral SNS axons. Control mice received the antagonist desipramine with 6-OHDA. DTH to TNP was measured by swelling of a footpad 24hr after epicutaneous challenge with picryl chloride (PCl). Anti-TNP antibodies were measured by ELISA. Splenic immunoregulatory effector cells were measured by the injection of AC-SPL into the footpad immediately after epicutaneous challenge with PCl. Results: AC-Thyreg from mice receiving intracameral TNP-BSA induced AC-SPL cells in recipients immunized systemically with TNP-BSA but not in naive mice or mice immunized with BSA or ovalbumin. ACAID ( measured as the suppression of DTH and the enhanced production of IgG1 antibodies specific for the intracameral antigen) was induced in mice immunized with 200µg of TNP-BSA but not in mice immunized with 20µg TNP-BSA. DTH was not expressed but IgM antibody production was enhanced in mice sympathectomized by the injection of 6-OHDA. Splenic immunoregulatory effector cells or AC-Thyreg were not recovered from sympathectomized mice receiving intracameral antigen. All of the sympathectomy effects were abrogated in control mice receiving desipramine in addition to 6-OHDA. Conclusions: The results provide additional evidence suggesting that immune deviation and the generation of splenic immunoregulatory T cells in ACAID depends on systemic immunzation. An intact sympathetic nervous system, (known to influence cell-mediated and humoral immunity), is required to generate AC-Thyreg and splenic immunoregulatory effector T cells in ACAID.

Keywords: ACAID • immune tolerance/privilege • immunomodulation/immunoregulation 
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