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Related Concept Videos

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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Catenins

Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
Catenins in Cell Junctions
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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
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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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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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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Cytokines regulate cysteine cathepsins during TLR responses.

Blaine M Creasy1, Kathleen L McCoy

  • 1Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298, USA. Blaine.Creasy@Stjude.org

Cellular Immunology
|December 15, 2010
PubMed
Summary

Toll-like receptor (TLR) activation in macrophages modulates cysteine cathepsin (Cat) B, L, and S activities. Cytokines induced by TLRs, such as TNF-α, IL-1β, and IFN-β, regulate these protease activities during inflammation.

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Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Toll-like receptor (TLR) activation is crucial for innate immunity but exacerbates inflammatory diseases.
  • Cysteine cathepsins (Cat B, L, S) are lysosomal proteases involved in physiological processes and upregulated in inflammation and cancer.
  • Macrophages, with high cathepsin expression, significantly contribute to inflammation and tissue damage in chronic inflammatory diseases.

Purpose of the Study:

  • To investigate the impact of Toll-like receptor (TLR) activation on macrophage cysteine cathepsin (Cat B, L, S) activities.
  • To elucidate the role of TLR-induced cytokines in regulating cathepsin proteolytic activity.

Main Methods:

  • Utilized live-cell enzymatic assays to measure intracellular cathepsin activities in macrophages.
  • Stimulated macrophages with TLR2, TLR3, and TLR4 ligands.
  • Assessed the effect of neutralizing antibodies against TNF-α, IL-1β, and IFN-β on cathepsin activity.

Main Results:

  • TLR2, TLR3, and TLR4 ligand stimulation differentially increased intracellular cathepsin B, L, and S activities.
  • TLR4-induced cytokines enhanced cathepsin proteolytic activity without altering mRNA expression of cathepsins or their inhibitors.
  • Neutralizing antibodies against TNF-α, IL-1β, and IFN-β differentially reduced cathepsin upregulation.

Conclusions:

  • Cytokines induced by both MyD88-dependent and -independent signaling pathways regulate macrophage cathepsin activities following TLR stimulation.
  • This highlights a novel mechanism by which TLRs influence macrophage function in inflammatory contexts.