01682nas a2200337 4500000000100000008004100001260001300042653002600055653002400081653002600105653002100131653001600152653001100168653002100179653001200200653001400212653002500226653001600251653001600267100002100283700001300304700001300317700001500330700001800345700001400363245006500377300001100442490000700453520087000460022001401330 1987 d c1987 Jun10aAntibodies, Bacterial10aAntigens, Bacterial10aChemotaxis, Leukocyte10aErythema Nodosum10aGlycolipids10aHumans10aImmunoglobulin M10aleprosy10aMonocytes10aMycobacterium leprae10aTemperature10aThalidomide1 aSchuller-Levis G1 aHarris D1 aCutler E1 aMeeker H C1 aHaubenstock H1 aLevis W R00aDefective monocyte chemotaxis in active lepromatous leprosy. a267-720 v553 a

This study of monocyte chemotaxis in leprosy patients showed a significant inverse correlation (p less than 0.05) of chemotaxis and the bacterial index (BI) (N = 22). In addition, there was a significant inverse correlation (p less than 0.05) between chemotaxis and the serum levels of anti-phenolic glycolipid-I IgM antibodies (N = 20). Patients taking thalidomide who had a BI greater than or equal to 1 had a significantly greater (p less than 0.001) chemotaxis response than that of patients with the same BI who were not taking thalidomide. No significant decrease in chemotaxis of monocytes from healthy donors was observed when the cells were pre-incubated with serum from 18 leprosy patients. We conclude that monocytes from patients with active lepromatous leprosy not receiving thalidomide have an intrinsic abnormality when assessed by chemotaxis.

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