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Related Concept Videos

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.
Naive T cells that have not yet encountered an antigen express two primary CD...
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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.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
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TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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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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The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

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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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Positive Regulator Molecules02:39

Positive Regulator Molecules

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Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
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Related Experiment Video

Updated: Mar 15, 2026

Characterization of Thymic Settling Progenitors in the Mouse Embryo Using In Vivo and In Vitro Assays
08:56

Characterization of Thymic Settling Progenitors in the Mouse Embryo Using In Vivo and In Vitro Assays

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Context-Specific Function of S6K2 in Th Cell Differentiation.

Christine Pai1, Craig M Walsh1, David A Fruman2

  • 1Department of Molecular Biology and Biochemistry, Institute for Immunology, University of California, Irvine, Irvine, CA 92697.

Journal of Immunology (Baltimore, Md. : 1950)
|September 11, 2016
PubMed
Summary
This summary is machine-generated.

p70 ribosomal protein S6 Kinase 2 (S6K2) is not essential for T cell differentiation or autoimmune responses. S6K2 loss did not impact experimental autoimmune encephalomyelitis, indicating its dispensability in this model.

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Directed Differentiation of Induced Pluripotent Stem Cells towards T Lymphocytes
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Directed Differentiation of Induced Pluripotent Stem Cells towards T Lymphocytes

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Related Experiment Videos

Last Updated: Mar 15, 2026

Characterization of Thymic Settling Progenitors in the Mouse Embryo Using In Vivo and In Vitro Assays
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Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • The mammalian target of rapamycin (mTOR) signaling pathway is crucial for T helper (Th) cell differentiation and proliferation.
  • mTOR complex-1 (mTORC1) is a key regulator, and its inhibition via rapamycin shows promise for autoimmune diseases.
  • Targeting downstream effectors of mTORC1 may offer more selective immunosuppression compared to direct mTORC1 inhibition.

Purpose of the Study:

  • To investigate the role of p70 ribosomal protein S6 Kinase 2 (S6K2), a downstream effector of mTORC1, in T cell function and autoimmunity.
  • To determine if S6K2 is essential for Th17 cell differentiation and experimental autoimmune encephalomyelitis (EAE).

Main Methods:

  • Utilized S6K2 knockout mice for genetic analysis.
  • Assessed T cell differentiation in vitro under different culture media conditions (RPMI 1640 vs. IMDM).
  • Evaluated disease progression and Th17 differentiation in vivo using a mouse model of experimental autoimmune encephalomyelitis (EAE).

Main Results:

  • S6K2 loss reduced Th17 cell differentiation and increased regulatory T cell differentiation in vitro when cultured in RPMI 1640 media.
  • S6K2 was found to be dispensable for Th17 differentiation in IMDM media.
  • S6K2 knockout mice showed no significant differences in clinical scores or Th17 differentiation in the EAE model compared to wild-type mice, even when rapamycin suppressed disease.

Conclusions:

  • S6K2 is dispensable for Th17-driven autoimmunity in the experimental autoimmune encephalomyelitis model.
  • Experimental conditions, such as cell culture media, significantly influence T cell differentiation outcomes.
  • S6K2 is not a critical target for modulating Th17-mediated autoimmune responses.