The present research tool is a knockout mouse model (FPR-/-) that lacks the high affinity N-formylpeptide receptor (FPR), created by targeted gene disruption.
This technology describes monoclonal antibodies against mouse chemokine (C-X-C motif) ligand 9 (CXCL9), also known as Monokine induced by gamma interferon (Mig). CXCL9 is a secreted protein that functions to attract white cells and increased expression of CXCL9 has been linked to several diseases. The inventors at the NIH generated over 100 anti-mouse CXCL9 antibodies from a CLXL9/Mig knockout mouse and further characterized several antibodies to show neutralization of CXCL9.
A plasmid encodes human fMLP receptor. Formyl peptide receptor (FPR, fMLP receptor) is a G protein-coupled receptor and mediates anti-inflammatory reactions in human neutrophils and other tissues.
A plasmid encodes human C-C motif chemokine receptor 3 (CCR3). It may contribute to the accumulation and activation of eosinophil and other inflammatory cells in the allergic airway.
A plasmid encodes human interleukin-8 (IL-8) receptor CXCR1. IL-8 is a chemo-attractant cytokine that attracts and activates neutrophils in inflammatory regions.
A plasmid encodes human CC chemokine receptor CX3CR1/CMKBRL1 as described in DNA Cell Biol. 1995 Aug;14(8):673-80, and developed in the laboratory of Philip M. Murphy at the National Institute of Allergy and Infectious Diseases.
Ulcerative colitis (UC) is a chronic inflammatory disease of the colorectum and affects approximately 400,000 people in the United States. The cause of UC is not known, although an abnormal immunological response to bacterial antigens in the gut microflora is thought to be involved. Present treatments for UC include anti-inflammatory therapy using aminosalicylates or corticosteroids, as well as immunomodulators and diet.
The nucleotide-binding oligomerization domain 2 (NOD2) protein plays a key role in innate immunity as a sensor of muramyl dipeptide (MDP), a breakdown product of bacterial peptidoglycan. Bacterial peptidoglycan promotes the innate immune response through the activation of Toll-like receptor 2 (TLR2), which ultimately provokes inflammation. Activation of NOD2 by MDP negatively regulates the activity of TLR2, and thus reduces inflammation.