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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755186/
[Above link to full text]
Ophthalmic Res. Author manuscript; available in PMC 2009 October 1.
Published in final edited form as:
Ophthalmic Res. 2008; 40(3-4): 193–199.
Published online 2008 April 18. doi: 10.1159/000119875. PMCID: PMC2755186
NIHMSID: NIHMS144378
Microbial Products Trigger Autoimmune Ocular Inflammation
Chiaki Fujimoto, Guangpu Shi, and Igal Gery
Laboratory of Immunology, National Eye Institute, NIH, Bethesda, Md., USA
Igal Gery, PhD, National Eye Institute, NIH, Building 10, Room 10N112, Bethesda, MD 20892-1857 (USA), Tel. +1 301 496 4159, Fax +1 301 480 1122, Email: geryi@nei.nih.gov
The publisher's final edited version of this article is available at Ophthalmic Res.
Abstract
Purpose:
Microbial products stimulate the immune system by interacting with Toll-like receptors (TLR) on antigen-presenting cells. This study examined the hypothesis that microbial products, which function as TLR ligands, are playing a major role in triggering pathogenic autoimmunity.
Methods:
An experimental system was developed in which microbial TLR ligands were tested in vivo for their capacity to stimulate naïve CD4 cells specific against hen egg lysozyme (HEL) to become effector cells capable of inducing inflammation in eyes in which HEL is expressed. The ligands’ mode of action was analyzed by determining their effects on the proliferation, acquisition of tissue-invading capacity, i.e. elevated CD49d and decreased CD62L expression, and production of interferon-γ by the HEL-specific cells.
Results:
All the 7 tested TLR ligands triggered ocular inflammation in the experimental system used here, with pertussis toxin surpassing all other ligands in its activities. A correlation was found between the capacity of the ligands to trigger pathogenic immunity and to stimulate the proliferation, modification of cell surface and interferon-γ production by T cells.
Conclusions:
This study provides direct evidence to support the notion that microbial products are capable of triggering pathogenic autoimmunity.
[Above link to full text]
Ophthalmic Res. Author manuscript; available in PMC 2009 October 1.
Published in final edited form as:
Ophthalmic Res. 2008; 40(3-4): 193–199.
Published online 2008 April 18. doi: 10.1159/000119875. PMCID: PMC2755186
NIHMSID: NIHMS144378
Microbial Products Trigger Autoimmune Ocular Inflammation
Chiaki Fujimoto, Guangpu Shi, and Igal Gery
Laboratory of Immunology, National Eye Institute, NIH, Bethesda, Md., USA
Igal Gery, PhD, National Eye Institute, NIH, Building 10, Room 10N112, Bethesda, MD 20892-1857 (USA), Tel. +1 301 496 4159, Fax +1 301 480 1122, Email: geryi@nei.nih.gov
The publisher's final edited version of this article is available at Ophthalmic Res.
Abstract
Purpose:
Microbial products stimulate the immune system by interacting with Toll-like receptors (TLR) on antigen-presenting cells. This study examined the hypothesis that microbial products, which function as TLR ligands, are playing a major role in triggering pathogenic autoimmunity.
Methods:
An experimental system was developed in which microbial TLR ligands were tested in vivo for their capacity to stimulate naïve CD4 cells specific against hen egg lysozyme (HEL) to become effector cells capable of inducing inflammation in eyes in which HEL is expressed. The ligands’ mode of action was analyzed by determining their effects on the proliferation, acquisition of tissue-invading capacity, i.e. elevated CD49d and decreased CD62L expression, and production of interferon-γ by the HEL-specific cells.
Results:
All the 7 tested TLR ligands triggered ocular inflammation in the experimental system used here, with pertussis toxin surpassing all other ligands in its activities. A correlation was found between the capacity of the ligands to trigger pathogenic immunity and to stimulate the proliferation, modification of cell surface and interferon-γ production by T cells.
Conclusions:
This study provides direct evidence to support the notion that microbial products are capable of triggering pathogenic autoimmunity.