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Related Concept Videos

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
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.
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Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
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.
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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...

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Related Experiment Video

Updated: Jun 21, 2026

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
04:44

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease

Published on: June 16, 2020

Innate immunity and inflammation in systemic sclerosis.

Robert Lafyatis1, Michael York

  • 1Rheumatology Section, Boston University School of Medicine, Boston, Massachusetts 02118, USA.

Current Opinion in Rheumatology
|July 28, 2009
PubMed
Summary

Innate immune sensors, like toll-like receptors (TLRs) and inflammasomes, drive autoimmunity and fibrosis in systemic sclerosis (SSc). Targeting these pathways offers new therapeutic strategies for SSc.

Area of Science:

  • Immunology
  • Pathology
  • Rheumatology

Background:

  • Innate immunity and inflammation are crucial in understanding autoimmunity and fibrosis.
  • Systemic sclerosis (SSc) pathogenesis involves complex interactions between immune responses and fibrotic processes.

Purpose of the Study:

  • To explore the role of innate immune sensors in systemic sclerosis (SSc).
  • To elucidate the connection between innate immunity, inflammation, and fibrosis in SSc.

Main Methods:

  • Review of recent advances in innate immunity and inflammation research.
  • Analysis of studies on toll-like receptors (TLRs), inflammasomes, and interferon-responsive genes (IRGs).

Main Results:

  • Nucleic acid immune complexes activate TLRs, inducing IRGs and autoantibodies in systemic lupus erythematosus (SLE) and potentially SSc.

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  • Inflammasome activation (NALP3) and inflammatory mediators (IL-1, IL-6, TNF-α) contribute to fibrosis.
  • Cooperation between TLR and non-TLR pathways may upregulate fibrotic mediators like TGF-β and IL-13.

    • Conclusions:

    • Innate immune pathways provide a new framework for understanding SSc.
    • Therapeutics targeting TLRs, IFN, and inflammasomes are under investigation.
    • Further research into inflammasome-mediated fibrosis could reveal novel SSc insights.