Abstract
A sample of 20 children with juvenile rheumatoid arthritis and 23 matched controls were studied in an attempt to verify null hypothesis that Mo function in children with JRA did not differ from that observed among healthy controls. The suppressor activity of Mo was studied by inhibition of 3H-thymidine incorporation in coculture with control PBMC stimulated with PHA. Functional expression of Fc receptor (FcR) was determined by EA rosettes, whereas expression of MHC class II determinants was assesed with HAK-75 and 14-4-4s mAb. It was shown that patients' Mo provided no appreciable suppression of PBMC stimulated with PHA. A significant (p <0.05) decrease of Mo (FcR+) in patients blood was observed. The number of Mo revealing HLA-DR determinants reacting with HAK-75 mAb was similar in both groups of children. However, the population of Mo with Ia. 7 receptor identified by 14-4-4s mAb was significantly (p < 0.05) diminished among the patients. A decreased Mo suppressor activity combined with decreased expressivity of Fc and Ia. 7 receptors justify the rejection of null hypothesis and imply an abnormal regulatory function of Mo in children with JRA.
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Szydlowska, T., Uracz, W., Ruggiero, I. et al. 129: MONOCYTE (Mo) FUNCTION IN CHILDREN WITH JUVENILE RHEUMATOID ARTHRITIS (JRA). Pediatr Res 24, 282 (1988). https://doi.org/10.1203/00006450-198808000-00154
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DOI: https://doi.org/10.1203/00006450-198808000-00154