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T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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TGF - β Signaling Pathway01:16

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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Receptor Downregulation in MVBs01:15

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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
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GPCRs Regulate Adenylyl Cylase Activity01:09

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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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Cytotoxic T Cells-mediated Immune Response01:27

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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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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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FcγRIIIa-Syk Co-signal Modulates CD4+ T-cell Response and Up-regulates Toll-like Receptor (TLR) Expression.

Anil K Chauhan1, Terry L Moore2, Ye Bi2

  • 1From the Division of Adult and Pediatric Rheumatology, Saint Louis University School of Medicine, St. Louis, Missouri 63104 chauhana@slu.edu.

The Journal of Biological Chemistry
|November 20, 2015
PubMed
Summary

Immune complexes in systemic lupus erythematosus (SLE) patients activate CD4(+) T-cells via FcγRIIIa, promoting pathogenic IL-17A and IFN-γ production. This FcγRIIIa-Syk signaling pathway influences adaptive immunity and toll-like receptor expression.

Keywords:
Fc-γ receptorT helper cellsautoimmunityinterferontoll-like receptor (TLR)

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmune Diseases

Background:

  • CD4(+) T-cells in systemic lupus erythematosus (SLE) exhibit aberrant T-cell receptor signaling involving Fc-receptor γ-chain Syk.
  • The specific role of FcγRIIIa activation by immune complexes (ICs) and complement C5b-9 in CD4(+) T-cell responses in SLE remains unexplored.

Purpose of the Study:

  • To investigate the mechanism by which ICs activate CD4(+) T-cells in SLE patients.
  • To determine if FcγRIIIa ligation by ICs can provide co-stimulatory signals to CD4(+) T-cells and induce pathogenic cytokine production.

Main Methods:

  • Analysis of CD4(+) T-cell activation markers and cytokine production in response to ICs from SLE patients.
  • Assessment of Syk phosphorylation (pSyk) and co-stimulatory signaling pathways (FcγRIIIa vs. CD28).
  • Gene expression analysis of IFN pathways, toll-like receptors (TLRs), HMGB1, and MyD88.

Main Results:

  • ICs from SLE patients bind to FcγRIIIa on CD4(+) T-cells, leading to Syk phosphorylation and co-stimulation independent of CD28.
  • This FcγRIIIa-Syk signaling drives the development of pathogenic IL-17A(+) and IFN-γ(high) CD4(+) T-cells in vitro, requiring IL-1β, IL-6, TGF-β1, and IL-23.
  • FcγRIIIa-mediated signaling differentially up-regulates IFN pathway genes and TLRs, with ICs co-localizing with TLR pathway proteins.

Conclusions:

  • FcγRIIIa ligation by ICs provides a crucial co-stimulatory signal to CD4(+) T-cells in SLE.
  • This pathway contributes to the pathogenesis of SLE by promoting the generation of pathogenic T-cell subsets.
  • The FcγRIIIa-Syk axis plays a significant role in modulating adaptive immune responses and TLR signaling in SLE.