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T Cell Types and Functions01:24

T Cell Types and Functions

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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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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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Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
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Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
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Inflammatory Bowel Disease II: Crohn's Disease01:30

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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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Analysis of Raw and Processed Cyperi Rhizoma Samples Using Liquid Chromatography-Tandem Mass Spectrometry in Rats with Primary Dysmenorrhea
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Curcumol reprograms the psoriatic microenvironment by interrupting the IL-36-NLRP3-NETs inflammatory circuit.

Shu-Lin Quan1, Zhi-Hong Zhang1, Ying-Mei An1

  • 1Key Laboratory of Traditional Chinese Korean Medicine Research of State Ethnic Affairs Commission, College of Pharmacy, Yanbian University, Yanji, Jilin Province, 133002, China; Key Laboratory of Natural Medicines of the Changbai Mountain, Ministry of Education, College of Pharmacy, Yanbian University, Yanji, Jilin Province, 133002, China.

Biochemical and Biophysical Research Communications
|November 18, 2025
PubMed
Summary

Curcumol, derived from Rhizoma Curcumae, effectively treats psoriasis by targeting key inflammatory pathways. It reduces skin inflammation and reshuffles the immune response, offering a promising multi-target therapy for this chronic condition.

Keywords:
CurcumolIL-36NLRP3Psoriasis

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Area of Science:

  • Immunology
  • Dermatology
  • Pharmacology

Background:

  • Psoriasis is a chronic, immune-mediated skin disease with complex pathogenesis.
  • Current treatments face challenges due to the multifactorial nature of psoriasis.
  • Curcumol, a sesquiterpenoid from Rhizoma Curcumae, possesses anti-inflammatory and immunomodulatory effects.

Purpose of the Study:

  • To investigate the therapeutic potential of curcumol in psoriasis.
  • To elucidate the mechanisms by which curcumol modulates inflammatory pathways in psoriasis.

Main Methods:

  • Investigated curcumol's effect on fibroblast-keratinocyte crosstalk.
  • Utilized an ex vivo model to study the IL-36γ-NLRP3 inflammasome axis.
  • Employed an imiquimod-induced murine psoriasis model to assess curcumol's in vivo efficacy.

Main Results:

  • Curcumol suppressed Poly(I:C)/LPS-induced IL-36α, IL-36γ, and NLRP3 inflammasome activation.
  • Curcumol disrupted the IL-36γ-NLRP3 inflammasome self-amplifying loop.
  • In vivo, curcumol ameliorated skin inflammation, restored keratinocyte differentiation, and reduced neutrophil and macrophage infiltration by targeting inflammasome activation and neutrophil NETosis.

Conclusions:

  • Curcumol alleviates psoriatic pathology through coordinated modulation of the IL-36γ-NLRP3-NETs inflammatory circuit.
  • Curcumol demonstrates potential as a novel multi-target therapeutic strategy for psoriasis management.