Related Experiment Video

Updated: Mar 2, 2026

A Macrophage Reporter Cell Assay to Examine Toll-Like Receptor-Mediated NF-kB/AP-1 Signaling on Adsorbed Protein Layers on Polymeric Surfaces
07:55

A Macrophage Reporter Cell Assay to Examine Toll-Like Receptor-Mediated NF-kB/AP-1 Signaling on Adsorbed Protein Layers on Polymeric Surfaces

Published on: January 7, 2020

7.9K

Allograft Inflammatory Factor-1 Links T-Cell Activation, Interferon Response, and Macrophage Activation in Chronic

Anne H Rowley1,2,3, Susan C Baker4, Kwang-Youn A Kim5

  • 1Departments of Pediatrics.

Journal of the Pediatric Infectious Diseases Society
|May 16, 2017
PubMed

Insights

Persistent immune responses, including T lymphocytes and type I interferon, are found in chronic Kawasaki disease (KD) arteritis. Allograft inflammatory factor-1 (AIF1) links these responses and macrophage activation, suggesting its role in KD pathogenesis.

Area of Science:

  • Immunology
  • Cardiovascular Pathology
  • Pediatric Rheumatology

Background:

  • Kawasaki disease (KD) is primarily viewed as acute arteritis, but chronic inflammation and arterial stenosis can persist.
  • Acute KD tissues show upregulated T lymphocyte, type I interferon, and allograft inflammatory factor-1 (AIF1) genes.
  • The persistence of these immune responses and the role of AIF1 in chronic KD are not well understood.

Purpose of the Study:

  • To determine if immune responses identified in acute KD persist in chronic KD arteritis.
  • To investigate the role of allograft inflammatory factor-1 (AIF1) in chronic KD immune responses.

Main Methods:

  • Gene and protein expression analysis (RT-PCR, immunohistochemistry, immunofluorescence) in chronic KD and control arteries.
  • In vitro studies using AIF1 small-interfering RNA to assess AIF1's role in macrophage and T lymphocyte activation.

Main Results:

  • Allograft inflammatory factor-1 (AIF1) protein is highly expressed in stenotic KD arteries, co-localizing with macrophages.
  • Genes related to T lymphocyte and interferon pathways remain significantly upregulated in chronic KD coronary arteries.
  • AIF1 is crucial for macrophage activation (CD80, MHC class II expression) and subsequent antigen-specific T lymphocyte activation.

Conclusions:

  • Allograft inflammatory factor-1 (AIF1) is significantly upregulated in KD stenotic arteries, indicating its involvement beyond acute phases.
  • Persistent T lymphocyte and type I interferon responses are characteristic of chronic KD arteritis.
  • AIF1 likely bridges type I interferon signaling, macrophage activation, and T lymphocyte responses, highlighting lymphocyte-myeloid cell crosstalk in KD pathogenesis and potential therapeutic targets.
Abstract

Keywords:
Kawasaki diseaseallograft inflammatory factor-1arteritis

More Related Videos

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis07:05

Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis

Published on: May 17, 2015

9.0K
Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro07:51

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

6.4K

Related Concept Videos

Inflammation01:38

Inflammation

Overview
62.9K
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
17.6K
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
2.9K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
13.4K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
10.1K
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
17.4K