Scientists Identify Rogue Immune Cells Driving Inflammation

Key Takeaways

  • Scientists identify specific immune cells driving inflammation
  • Discovery could lead to safer, targeted treatments for chronic diseases
  • “Rogue” neutrophils cause tissue damage in conditions like fatty liver and rheumatoid arthritis

Scientists have discovered specific immune cells responsible for driving inflammation, opening doors to more precise treatments for chronic inflammatory and autoimmune conditions.

The Role of Neutrophils in Inflammation

The human blood contains three major cell types: red blood cells, white blood cells, and platelets. White blood cells serve as the body’s primary immune defense, fighting infections from bacteria, viruses, and parasites.

Neutrophils constitute 60-70% of white blood cells and play a crucial role. They engulf pathogens, release cytokines to summon other immune cells, and clear cellular debris after infection.

However, when neutrophils become overactive or remain too long, they trigger inflammation leading to diseases including fatty liver, rheumatoid arthritis, lupus, and severe COVID-19 cases.

“Neutrophils play a critical role in various patho-physiological conditions. However, their therapeutic targeting has been challenging due to the associated risk of infections. Therefore, identifying disease-associated neutrophil populations is essential for targeted strategies,” the study published in Cell Reports states.

Discovery of “Rogue” Neutrophils

A CSIR Central Drug Research Institute team led by Dr. Sachin Kumar found that not all neutrophils are equal. A sub-group lives longer and causes more aggressive inflammation.

These “rogue” neutrophils are particularly abundant in the liver and appear in both short-term and long-term inflammatory conditions. While regular neutrophils fight infection, persistent rogue neutrophils cause more tissue damage.

Research Methods and Findings

Using advanced techniques including high-resolution microscopy and cell sorting, researchers observed that inflammatory signals and metabolic stress can transform regular neutrophils into rogue versions.

These cells store more lipids and fats, suggesting their activity is influenced by fat metabolism changes. When researchers blocked the rogue protein on these cells, harmful effects like tissue damage and excess inflammation reduced significantly.

The study reveals a distinct neutrophil subpopulation with unique functional attributes.

“By establishing their presence and relevance in inflammatory settings, our findings significantly advance the understanding of neutrophil heterogeneity and function,” the researchers said.

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