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Related Experiment Video

Updated: Feb 14, 2026

Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels

Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels

Published on: August 7, 2017

Negative regulators that mediate ocular immune privilege.

Andrew W Taylor¹, Tat Fong Ng¹

¹Boston University School of Medicine, Boston, Massachusetts, USA.

Journal of Leukocyte Biology

|February 13, 2018

Summary

This summary is machine-generated.

The eye uses molecules like TGF-β2 and immune cells to control inflammation, maintaining vision health and immune privilege. This discovery offers new avenues for treating autoimmune diseases by harnessing these natural regulators.

Keywords:

Immunosuppression anti-inflammatory eye neuropeptides regulatory T cells suppressor macrophages tolerance

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Last Updated: Feb 14, 2026

Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels

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Published on: August 7, 2017

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Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

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Published on: June 24, 2020

Area of Science:

Ophthalmology
Immunology
Molecular Biology

Background:

The eye possesses unique immune privilege to protect vision.
Inflammation can compromise ocular health and visual function.

Purpose of the Study:

To identify and characterize negative regulators of inflammation in the ocular microenvironment.
To understand the role of these regulators in maintaining immune privilege and tolerance.
To explore their potential for treating ocular autoimmune diseases.

Main Methods:

Analysis of constitutively produced negative regulators in the eye.
Investigating the influence of TGF-β2, α-MSH, FasL, and PD-L1 on inflammatory pathways.
Assessing the impact on immune cell activation and regulation under inflammatory conditions.

Main Results:

Identified key molecular regulators (TGF-β2, α-MSH, FasL, PD-L1) that suppress ocular inflammation.
Demonstrated that these regulators prevent effector immune cell activation.
Showed that these molecules promote regulatory immune cells, enhancing immune tolerance.

Conclusions:

Ocular immune privilege involves both molecular and cellular negative regulators of inflammation.
These regulators are crucial for preventing and resolving ocular inflammation.
Harnessing these negative regulators presents a promising strategy for novel autoimmune disease therapies.