June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Analysis of chemokines involved in the pathogenesis of dacryoadenitis in mice deficient for programmed cell death-1
Author Affiliations & Notes
  • Yutaka Sakurai
    national defense medecal college, Tokorozawa, Japan
  • Masataka Ito
    national defense medecal college, Tokorozawa, Japan
  • Yoko Karasawa
    national defense medecal college, Tokorozawa, Japan
  • Yoshihiko Usui
    tokyo medical university, tokyo, Japan
  • Takaaki Hattori
    tokyo medical university, tokyo, Japan
  • Hiroshi Goto
    tokyo medical university, tokyo, Japan
  • Masaru Takeuchi
    national defense medecal college, Tokorozawa, Japan
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 918. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Yutaka Sakurai, Masataka Ito, Yoko Karasawa, Yoshihiko Usui, Takaaki Hattori, Hiroshi Goto, Masaru Takeuchi; Analysis of chemokines involved in the pathogenesis of dacryoadenitis in mice deficient for programmed cell death-1. Invest. Ophthalmol. Vis. Sci. 2013;54(15):918.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: Programmed cell death-1 (PD-1, pdcd1) is one of the costimulatory molecules, negatively regulates the immune responses. Previously, we reported that PD-1-deficient C57BL/6 mice spontaneously develop sjogren syndrome-like dacryoadenitis from 3 months after birth.In this study, we investigated chemokines expression in the lacrimal gland (LG) of pdcd1-/- mice to characterize T cells involved in the development.

Methods: The LG were obtained from C57BL/6 pdcd1+/+ and pdcd1-/- mice at 4-,6-,or 12-month-old. The production of CCL1, CCL2, CCL3, CCL4, CCL5, CCL11, CCL12, CCL17, CXCL1, CXCL2, CXCL9, CXCL10, CXCL11, CXCL12, and CXCL13 in the LG of 4-,6-,or 12-month-old pdcd1-/- mice and 4-month-old pdcd1+/+ mice were measured by mouse cytokine array A kit (R&D system). In addition, mRNAs were extracted from the LG, and mRNA expression of CCL3, CCL5, CCL20, CCL22, CXCL9, and CXCL10 in the LG of 4-month-old pdcd1-/- mice and pdcd1+/+ mice were analyzed by real-time PCR.

Results: CCL3, CCL5, CXCL9, and CXCL10 associated with Th1 cell migration were produced in the LG of pdcd1-/- mice compared to pdcd1+/+ mice at 4-month-old. Production of these chemokines related to Th1 cells in the LG of pdcd1-/- mice increased with aging. In the mRNA expression, Pdcd1-/- mice had significantly higher levels of CCL3, CCL5, CXCL9, CXCL10 related to Th1 cells, and CCL20 related to Th17 cells mRNA transcripts in the LG than pdcd1+/+ mice at 4-month-old. Especially, mRNA expression of CCL20 was remarkably higher than others. mRNA expression of CCL22 related to Th2 cells were also detected, but was apparently lower than others.

Conclusions: These results indicate that Th1- and Th17-mediated immune responses are involved in the development of dacryoadenitis in Pdcd1-/- mice, and that Th17 cells play a pivotal role in the pathogenesis.

Keywords: 432 autoimmune disease • 576 lacrimal gland  
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×