The Indian Rheumatology Association

The Professional Organization of Rheumatologists and other Health Professionals in India

Basic Science

Basic Science
Compiled By

ARVIND G

MD DM (Immunology & Rheumatology)
Assistant Professor
CMC Vellore

DEBANJALI SINHA
MD (Med)
MRCP (UK)
DM (Rheumatology)
Consultant Physician and Rheumatologist

dc

SLE


Role of NETosis

Last 3 months a number of papers were published looking at NETosis. TLR7 and role of B cells in lupus. Starting with B cells, a distinct subset of B cells was identified where authors showed The authors show that extra-follicular autoreactive CD27- IgD- CXCR5- CD11c+ (Double Negative) B cells, are expanded in lupus patients. These cells demonstrate hyper-responsivess to innate activation by TLR 7 mediated mechanisms and generative auto-reactive plasmablasts. [1] .

In another study authors tried discriminating canonical and non-canonical pathway leading to NETosis as former which is NOX dependent has less capacity to activate endothelial cells. In the canonical pathway of NET release, often referred to as nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX)-dependent or lytic NET formation, the assembly of NOX at cytoplasmic or phagosomal membranes and the subsequent generation of reactive oxygen species (ROS) initiates a series of events which culminate in explosive cell death accompanied by NET release. In the non-canonical pathway, i.e. NOX-independent NET formation, neutrophils are not lysed, but instead they release NETs through blebbing of the nuclear envelope and the subsequent vesicular inside-out transportation of NETs. Activated platelets appear to be potent inducers of NOX-independent NET formation.

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