Related Experiment Video
Updated: May 11, 2026
04:39
Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
Published on: March 17, 2023
Serum LAIR-2 is increased in autoimmune thyroid diseases
Rita Simone1, Giampaola Pesce, Princey Antola
1Department of Experimental Medicine - Section of Human Anatomy, University of Genova, Genova, Italy.
Plos One
|May 22, 2013
Summary
High levels of soluble Leukocyte-associated Ig-like receptor-2 (LAIR-2) were found in patients with autoimmune thyroid diseases. Serum LAIR-2 can bind collagen and may regulate the inhibitory function of LAIR-1.
Area of Science:
- Immunology
- Endocrinology
- Molecular Biology
Background:
- Leukocyte-associated Ig-like receptors (LAIRs) are a family of receptors that inhibit immune cell function through collagen binding.
- LAIR-1 is an inhibitory receptor found on immune cells, while LAIR-2 is a soluble homolog.
- Research has primarily focused on LAIR-1, with limited investigation into LAIR-2's expression and function.
Purpose of the Study:
- To investigate the expression and potential function of LAIR-2 in autoimmune thyroid diseases.
- To determine the relationship between serum LAIR-2 levels and clinical manifestations of autoimmune thyroid diseases.
- To explore the in vitro binding capabilities of serum LAIR-2 to its natural ligand, collagen.
Main Methods:
- Serum samples from patients with Graves' disease and autoimmune thyroiditis were analyzed for LAIR-2 levels.
- Correlation analysis was performed between LAIR-2 levels and clinical parameters, including thyroid function and ophthalmopathy.
- In vitro assays were conducted to assess the binding affinity of serum LAIR-2 to collagen.
Main Results:
- Elevated LAIR-2 levels were detected in a high percentage (74/80) of sera from patients with autoimmune thyroid diseases.
- LAIR-2 levels did not correlate with specific clinical manifestations, thyroid function status, or ophthalmopathy.
- Serum LAIR-2 demonstrated in vitro binding to collagen, with a higher affinity compared to LAIR-1.
Conclusions:
- Soluble LAIR-2 is significantly elevated in patients with autoimmune thyroid diseases.
- Serum LAIR-2 retains its ability to bind collagen.
- LAIR-2 may play a regulatory role in immune responses within autoimmune thyroid diseases, potentially by modulating LAIR-1 function due to its higher collagen affinity.
Related Concept Videos
01:24Graves Disease II: Pathophysiology
Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
01:28Graves' Disease I: Introduction
Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
01:27Hyperthyroidism II: Pathophysiology
Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
01:20Synthesis and Regulation of Thyroid Hormones
Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
01:25Hyperthyroidism I: Introduction
Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
01:23Hypothyroidism II: Pathophysiology
Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...