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Inflammation

Inflammation

Intracellular Signaling Affects Focal Adhesions

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...

Porin Insertion in the Outer Mitochondrial Membrane

Porin Insertion in the Outer Mitochondrial Membrane

Porins are beta-barrel proteins translocated to the mitochondrial outer membrane through the TOM complex into the intermembrane space. Porin precursors bind TIM chaperones within the intermembrane space and are guided to the Sorting and Assembly Machinery complex or SAM complex on the outer mitochondrial membrane.
Three models describe the assembly of porins by the SAM complex and their insertion into the outer membrane. Model 1 suggests that porins are assembled outside the SAM channel as the...

Insertion of Single-pass Transmembrane Proteins in the RER

Insertion of Single-pass Transmembrane Proteins in the RER

Integral membrane proteins are proteins adhered to the lipid bilayer of a cell organelle or membrane. They can be of two types: transmembrane integral proteins that span the lipid bilayer and monotopic proteins that are attached to either side of the membrane but do not pass through it.
Integral transmembrane proteins possess transmembrane and extra membrane domains. The transmembrane domains are primarily made of 20-25 hydrophobic amino acids arranged in a helical secondary confirmation. These...

Insertion of Multi-pass Transmembrane Proteins in the RER

Insertion of Multi-pass Transmembrane Proteins in the RER

The rough ER membrane synthesizes, assembles, and embeds transmembrane proteins in diverse topologies. These proteins function as transporters or channels and can remain in the ER membrane or are sent to the Golgi complex, lysosome, and cell membrane.
The multipass transmembrane proteins are the type IV integral membrane proteins with multiple topogenic sequences determining their spatial arrangement in the ER membrane. Nearly all multipass proteins lack a cleavable signal sequence and use...

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A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

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Enthesitis: Much More Than Focal Insertion Point Inflammation.

Abdulla Watad^1,2,3, Richard J Cuthbert³, Howard Amital^1,2

¹Department of Medicine 'B', Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Ramat Gan, Israel.

Current Rheumatology Reports

|May 31, 2018

Summary

Enthesitis is a key factor in spondyloarthropathies (SpA). Research highlights its role in SpA development and inflammation, supported by animal models and human studies.

Keywords:

Entheses Enthesitis IL-12 IL-17 IL-23 JAKi

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Area of Science:

Rheumatology
Immunology
Pathology

Background:

Enthesitis is increasingly recognized as central to spondyloarthropathies (SpA).
Understanding the pathogenic role of enthesitis in SpA is crucial for developing effective treatments.

Purpose of the Study:

To summarize current knowledge on the pathogenic role of enthesitis in spondyloarthropathies (SpA).
To review findings from both animal models and human studies regarding enthesitis in SpA.

Main Methods:

Review of experimental models of SpA-like diseases.
Analysis of human in vivo studies investigating enthesitis.
Examination of data from studies using JAK, IL-17, and IL-23 inhibitors.

Main Results:

Experimental models demonstrate SpA-like diseases originating at entheses, associated with nail disease and dactylitis.
Enthesitis is a critical, though often indirectly assessed, parameter in SpA, including ankylosing spondylitis.
Targeting pathways involving JAK, IL-17, and IL-23 provides insights into enthesitis mechanisms.

Conclusions:

Enthesitis and enthesis organ inflammation are likely primary drivers of skeletal inflammation in SpA.
Emerging research is elucidating the molecular basis of enthesitis-driven joint inflammation in SpA.