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The role of ACAID and CD4+CD25+FOXP3+ regulatory T cells on CTL function against MHC alloantigens.

Publication ,  Journal Article
Saban, DR; Cornelius, J; Masli, S; Schwartzkopff, J; Doyle, M; Chauhan, SK; Peck, AB; Grant, MB
Published in: Mol Vis
2008

PURPOSE: Anterior chamber associated immune deviation (ACAID) is an antigen-specific form of peripheral immune tolerance that is induced to exogenous antigens placed in the ocular anterior chamber, which leads to a suppression in delayed-type hypersensitivity (DTH). Considerable work has been done on ACAID induction to major histocompatibility (MHC) alloantigens. However, its role on cytotoxic T lymphocyte (CTL) activity is currently unknown. METHODS: C57BL/6 (H-2(b)) mice received an intracameral (IC) inoculation with BALB/c (H-2(d)) splenocytes. Splenic CD4(+) and CD8(+) T cell populations were characterized by flow cytometry and proliferation assays during induction and expression phases of ACAID. Percentages of CD4(+)CD25(+)FoxP3(+) T regulatory cells (Treg) were also followed. Lastly, CTL function was measured at various time points during ACAID expression, and Treg were added to identify potential alterations in CTL function. RESULTS: CD4(+) and CD8(+) T cell percentages and proliferation increased in the spleen during ACAID induction but then sharply decreased in response to an allospecific immunization. Expression of ACAID also exhibited a significant drop in CTL function. However, while Treg expansion was observed, these cells did not directly mediate the CTL inhibition. CONCLUSIONS: ACAID mediates an inhibition of CTL function against MHC alloantigens. Furthermore, we found that ACAID induction leads to the expansion and proliferation of CD4(+) and CD8(+) T cells while ACAID expression is associated with a diminishment in T cell percentages due to proliferation impairment. Lastly, Treg also expand during ACAID induction. However, our data suggest that Treg do not directly inhibit CTL activity.

Duke Scholars

Published In

Mol Vis

EISSN

1090-0535

Publication Date

2008

Volume

14

Start / End Page

2435 / 2442

Location

United States

Related Subject Headings

  • T-Lymphocytes, Regulatory
  • T-Lymphocytes, Cytotoxic
  • Spleen
  • Ophthalmology & Optometry
  • Mice, Inbred C57BL
  • Mice, Inbred BALB C
  • Mice
  • Lymphocyte Subsets
  • Isoantigens
  • Interleukin-2 Receptor alpha Subunit
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Saban, D. R., Cornelius, J., Masli, S., Schwartzkopff, J., Doyle, M., Chauhan, S. K., … Grant, M. B. (2008). The role of ACAID and CD4+CD25+FOXP3+ regulatory T cells on CTL function against MHC alloantigens. Mol Vis, 14, 2435–2442.
Saban, Daniel R., Janet Cornelius, Sharmila Masli, Johannes Schwartzkopff, Maire Doyle, Sunil K. Chauhan, Ammon B. Peck, and Maria B. Grant. “The role of ACAID and CD4+CD25+FOXP3+ regulatory T cells on CTL function against MHC alloantigens.Mol Vis 14 (2008): 2435–42.
Saban DR, Cornelius J, Masli S, Schwartzkopff J, Doyle M, Chauhan SK, et al. The role of ACAID and CD4+CD25+FOXP3+ regulatory T cells on CTL function against MHC alloantigens. Mol Vis. 2008;14:2435–42.
Saban, Daniel R., et al. “The role of ACAID and CD4+CD25+FOXP3+ regulatory T cells on CTL function against MHC alloantigens.Mol Vis, vol. 14, 2008, pp. 2435–42.
Saban DR, Cornelius J, Masli S, Schwartzkopff J, Doyle M, Chauhan SK, Peck AB, Grant MB. The role of ACAID and CD4+CD25+FOXP3+ regulatory T cells on CTL function against MHC alloantigens. Mol Vis. 2008;14:2435–2442.

Published In

Mol Vis

EISSN

1090-0535

Publication Date

2008

Volume

14

Start / End Page

2435 / 2442

Location

United States

Related Subject Headings

  • T-Lymphocytes, Regulatory
  • T-Lymphocytes, Cytotoxic
  • Spleen
  • Ophthalmology & Optometry
  • Mice, Inbred C57BL
  • Mice, Inbred BALB C
  • Mice
  • Lymphocyte Subsets
  • Isoantigens
  • Interleukin-2 Receptor alpha Subunit