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Autoimmune Disorders

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Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
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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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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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Inflammatory Bowel Disease II: Crohn's Disease01:30

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G Protein–Coupled Receptors (GPCRs) are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to various stimuli. GPCRs regulate critical physiological pathways and are excellent drug targets for treating diseases such as diabetes, cancer, obesity, depression, or Alzheimer's. Nearly 35% of approved drugs implement their therapeutic effects by selectively interacting with specific GPCRs.
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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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FcγRIIB and autoimmunity.

Marion Espéli1, Kenneth G C Smith2, Menna R Clatworthy2

  • 1Inserm UMR_S996, LabEx LERMIT, Université Paris-Sud, Paris, France.

Immunological Reviews
|December 20, 2015
PubMed
Summary

The inhibitory Fc gamma receptor IIB (FcγRIIB) regulates autoimmune diseases by controlling autoantibody production and immune cell activation. Emerging research reveals its crucial role in both adaptive and innate immunity.

Keywords:
Fcγ receptorsautoantibodiesdendritic cellsgerminal center B cellslymphangiogenesismacrophages

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Area of Science:

  • Immunology
  • Autoimmunity
  • Molecular Biology

Background:

  • Autoimmune diseases involve immune responses against self-antigens, leading to autoantibody production.
  • Autoantibodies trigger inflammation via complement activation and Fc gamma receptors (FcγRs).
  • The inhibitory Fc gamma receptor IIB (FcγRIIB) is key in regulating autoantibody generation and effector functions.

Purpose of the Study:

  • To review the role of FcγRIIB in adaptive immune responses in autoimmunity.
  • To highlight the emerging functions of FcγRIIB in innate immunity.
  • To update on novel mechanisms of FcγRIIB in immune regulation.

Main Methods:

  • Literature review of recent studies on FcγRIIB.
  • Analysis of FcγRIIB's role in B cell and dendritic cell regulation.
  • Examination of FcγRIIB's impact on innate immune receptor signaling.

Main Results:

  • FcγRIIB regulates germinal center B cells and dendritic cell migration, impacting autoimmunity.
  • FcγRIIB inhibits Toll-like receptor and complement receptor-mediated activation in innate immunity.
  • FcγRIIB polymorphisms are linked to autoimmunity susceptibility and infection protection.

Conclusions:

  • FcγRIIB is a critical regulator of both adaptive and innate immune responses in autoimmunity.
  • Understanding FcγRIIB's multifaceted roles offers therapeutic targets for autoimmune diseases.
  • Further research into FcγRIIB's mechanisms can advance autoimmune disease treatment.