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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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Immune Response Against Viral Pathogens01:29

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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The JAK-STAT Signaling Pathway01:20

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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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Autoimmune Disorders01:29

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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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Inflammatory Response01:28

Inflammatory Response

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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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What is the Immune System?01:38

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Related Experiment Video

Updated: Aug 8, 2025

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
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Systemic Lupus Erythematosus Pathogenesis: Interferon and Beyond.

Simone Caielli1, Zurong Wan1, Virginia Pascual1

  • 1Drukier Institute for Children's Health and Department of Pediatrics, Weill Cornell Medical Center, New York, NY, USA; email: sic2011@med.cornell.edu, zuw4001@med.cornell.edu, vip2021@med.cornell.edu.

Annual Review of Immunology
|February 28, 2023
PubMed
Summary
This summary is machine-generated.

Novel genetic insights reveal mitochondria

Keywords:
autoantibodiescell deathextrafollicularlupusmitochondria

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Area of Science:

  • Immunology and Genetics of Systemic Lupus Erythematosus (SLE)

Background:

  • Autoreactive B cells and interferons are key drivers of SLE pathogenesis.
  • Existing treatments targeting these pathways show partial success, indicating diverse upstream mechanisms.
  • Understanding these upstream drivers is crucial for developing more effective SLE therapies.

Purpose of the Study:

  • To review recent genetic and immune monitoring studies in SLE patients.
  • To elucidate novel upstream mechanisms contributing to SLE pathogenesis.
  • To explore the role of mitochondria and B cell abnormalities in SLE.

Main Methods:

  • Analysis of genetic studies identifying novel mutations in SLE.
  • Review of immune monitoring data from SLE patients.
  • Examination of mitochondrial dysfunction and nucleic acid metabolism in SLE.

Main Results:

  • Novel mutations affecting B cell activation and nucleic acid clearance identified.
  • Mitochondrial dysfunction identified as a key contributor to SLE pathogenesis.
  • Specific autoantibody profiles linked to genetic alterations and immune activation loops.

Conclusions:

  • Emerging insights into genetic and mitochondrial factors refine understanding of SLE.
  • Atypical B cells and novel T helper subsets contribute to autoantibody generation.
  • These findings support patient stratification and personalized therapeutic strategies for SLE.