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Related Concept Videos

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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Inflammation01:38

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Inflammatory Response I: Vascular and Cellular01:30

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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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.
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Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

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The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
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The Intrinsic Apoptotic Pathway01:31

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1&#946; using a Whole Blood Stimulation Assay
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Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1β using a Whole Blood Stimulation Assay

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The everchanging framework of autoinflammation.

Raffaele Manna1,2, Donato Rigante3,4

  • 1Department of Internal Medicine, Fondazione Policlinico A. Gemelli IRCCS, Rare Diseases and Periodic Fevers Research Centre, Università Cattolica Sacro Cuore, Largo A. Gemelli no. 8, 00168, Rome, Italy. raffaele.manna@policlinicogemelli.it.

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Summary
This summary is machine-generated.

Autoinflammatory disorders (AIDs) are immune system errors causing unexplained inflammation. This review highlights pediatric AIDs, focusing on recognition and new targeted therapies for better disease control.

Keywords:
AutoinflammationAutoinflammatory diseaseChildInflammasomeInflammasomopathyInnovative biotechnologiesInterferonInterleukin-1Nuclear factor-κBPersonalized medicineRecurrent fever

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Area of Science:

  • Immunology
  • Genetics
  • Pediatrics

Background:

  • Innate immunity protects against infection; errors lead to autoinflammatory disorders (AIDs).
  • AIDs involve aberrant inflammation without infection or autoimmunity, often with pediatric onset.
  • Dysregulated inflammasome, NF-κB, and interferon pathways are implicated in AIDs pathogenesis.

Purpose of the Study:

  • To review key autoinflammatory disorders in childhood.
  • To emphasize clinical features aiding in AIDs recognition.
  • To provide insights for young scientists on AIDs diagnosis and management.

Main Methods:

  • Literature review focusing on pediatric autoinflammatory disorders.
  • Analysis of clinical presentations and diagnostic challenges.
  • Summary of current and emerging therapeutic strategies.

Main Results:

  • AIDs present with diverse phenotypes, often misdiagnosed or diagnosed late.
  • Inflammasomopathies, NF-κB-related disorders, and interferonopathies are key AID categories.
  • Genomically-guided approaches offer targeted biologic therapies for improved disease control.

Conclusions:

  • Early recognition of AIDs in children is crucial for timely intervention.
  • Understanding AIDs' genetic and molecular basis informs targeted treatment strategies.
  • Advancements in therapy offer hope for better management and outcomes in pediatric AIDs.