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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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Overview
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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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Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

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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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Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

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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.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
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Related Experiment Video

Updated: Mar 21, 2026

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

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Inflammatory Mediators Both Directly and Indirectly Promote Microglial Proliferation.

Brady P Hammond1, Eugene Hahn1, Kelly V Lee1

  • 1Neuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada.

Glia
|March 20, 2026
PubMed
Summary
This summary is machine-generated.

Microglial proliferation, crucial for brain development and repair, is regulated by specific factors. This study identified colony stimulating factor-2, interleukin-3, and tumor necrosis factor-ɑ as direct microglial mitogens.

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Culturing Microglia from the Neonatal and Adult Central Nervous System
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Culturing Microglia from the Neonatal and Adult Central Nervous System
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Area of Science:

  • Neuroimmunology
  • Central Nervous System (CNS) Biology
  • Cellular Proliferation Mechanisms

Background:

  • Microglia are the primary immune cells in the CNS, essential for development and injury response.
  • Microglial proliferation increases cell density to fulfill critical functions.
  • The precise mechanisms and factors governing microglial proliferation are not fully understood.

Purpose of the Study:

  • To systematically screen and compare factors previously suggested to influence microglial proliferation.
  • To identify direct (mitogenic) and indirect regulators of microglial proliferation.
  • To elucidate the mechanisms underlying microglial density changes in the CNS.

Main Methods:

  • Screening of 22 potential mitogenic factors using serum-free microglial cultures.
  • Assessment of direct mitogenic effects of cytokines on microglia.
  • Testing indirect proliferation effects by conditioning media from other CNS cell lineages.

Main Results:

  • Colony stimulating factor-2 (CSF2), interleukin-3 (IL-3), and tumor necrosis factor-ɑ (TNF-ɑ) were confirmed as direct microglial mitogens.
  • Interleukin-1ɑ (IL-1ɑ) and interleukin-1β (IL-1β) induced astrocytes to release CSF2, a microglial mitogen.
  • Few previously reported factors directly or indirectly promoted microglial proliferation under standardized conditions.

Conclusions:

  • CSF2, IL-3, and TNF-ɑ are key direct regulators of microglial proliferation.
  • Astrocyte-derived CSF2, induced by IL-1ɑ and IL-1β, represents an indirect proliferation pathway.
  • This study provides a standardized comparison, revealing limited direct or indirect mitogenic factors for microglia.