Abstract
In leukocyte adhesion deficiency type I, neutrophils fail to adhere to blood vessel walls and thus cannot transmigrate to peripheral tissues. Leukocyte adhesion deficiency type I patients invariably experience an aggressive form of generalized periodontitis, which has been historically attributed to defective neutrophil surveillance of the periodontal infection. This time-honored notion has now been challenged by a recent study, which showed that the underlying etiology involves a dysregulated host response that leads to overexpression of the proinflammatory and bone-resorptive cytokine IL-17.
Keywords:
IL-17; inflammation; leukocyte adhesion deficiency; neutrophils; periodontitis.
Publication types
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Editorial
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Bacterial Infections / complications
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Bacterial Infections / immunology*
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Bone Resorption
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Chemotaxis
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Disease Models, Animal
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Humans
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Inflammation Mediators / metabolism
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Interleukin-17 / genetics
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Interleukin-17 / metabolism*
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Leukocyte-Adhesion Deficiency Syndrome / complications
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Leukocyte-Adhesion Deficiency Syndrome / immunology*
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Mice
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Molecular Targeted Therapy
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Neutrophils / immunology*
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Neutrophils / microbiology
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Periodontitis / etiology
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Periodontitis / immunology*
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Transendothelial and Transepithelial Migration
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Up-Regulation
Substances
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Inflammation Mediators
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Interleukin-17
Supplementary concepts
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Leukocyte adhesion deficiency type 1