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Related Concept Videos

Autoimmune Disorders01:29

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.
Concept and Mechanism of Autoimmune Diseases
The immune...
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T Cell Types and Functions01:24

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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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Antigens Involved in Adaptive Immunity01:26

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An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
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Tissue Transplantation01:24

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Tissue transplantation is a significant medical procedure involving the transfer of cells, tissues, or organs from a donor to a recipient, with the primary aim of restoring lost functions. This procedure is crucial in treating a broad spectrum of diseases, including kidney diseases, liver failure, heart disease, and certain types of cancers.
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mTOR Signaling and Cancer Progression03:03

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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mTORC2 contributes to systemic autoimmunity.

Xian Zhou1, Haiyu Qi1,2, Meilu Li1,3

  • 1Division of Rheumatology, Department of Medicine, Mayo Clinic Rochester, Minnesota, USA.

Immunology
|October 23, 2022
PubMed
Summary
This summary is machine-generated.

Mechanistic target of rapamycin complex 2 (mTORC2) drives autoimmune disease by promoting T-cell activation and differentiation. Inhibiting mTORC2 in T cells ameliorated disease, suggesting it as a therapeutic target for systemic autoimmunity.

Keywords:
T follicular helper cellautoimmunitylupus/SLEregulatory T cells

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmune Diseases

Background:

  • Systemic autoimmune diseases are linked to type I interferon (IFN) pathway overactivation, lymphopenia, and T follicular helper (Tfh) cell expansion.
  • The precise cellular and molecular drivers of these immune dysregulations are not fully elucidated.

Purpose of the Study:

  • To investigate the role of mechanistic target of rapamycin complex 2 (mTORC2) in Tfh cell differentiation and Treg homeostasis within the context of systemic autoimmunity.
  • To determine the therapeutic potential of targeting mTORC2 in autoimmune disease models.

Main Methods:

  • Utilized a systemic autoimmunity mouse model.
  • Genetically inactivated mTORC2 in total T cells and specifically in regulatory T cells (Tregs).
  • Assessed Tfh cell differentiation, B-cell activation, T-cell glucose metabolism, and T-cell lymphopenia.

Main Results:

  • mTORC2 inactivation in total T cells, but not Tregs, significantly reduced autoimmune immunopathology.
  • This amelioration correlated with decreased Tfh differentiation, B-cell activation, and T-cell glucose metabolism.
  • Type I IFN and T-cell receptor (TCR) signaling synergize to activate mTORC2 in T cells, contributing to lymphopenia.

Conclusions:

  • mTORC2 acts downstream of type I IFN, TCR, and ICOS signaling to regulate T-cell metabolism, Tfh differentiation, and lymphopenia in systemic autoimmunity.
  • mTORC2 does not appear to suppress Treg function in this context.
  • mTORC2 inhibition presents a promising therapeutic strategy for treating systemic autoimmune diseases.