02530nas a2200373   4500000000100000008004100001260001300042653001500055653001000070653001900080653001700099653001400116653001200130653002200142653003800164653001100202653001900213653001100232653001200243653002400255653000900279653001600288100001300304700001400317700001400331700001800345245007200363856006900435300001000504490000700514050001500521520160600536022001402142       2004                            d  c2004 Jan10aAdolescent10aAdult10aAutoantibodies10aAutoantigens10aCell Line10aCytosol10aEndothelial Cells10aEnzyme-Linked Immunosorbent Assay10aFemale10aFlow Cytometry10aHumans10aleprosy10aMalaria, Falciparum10aMale10aMiddle Aged1 aDugué C1 aPerraut R1 aYouinou P1 aRenaudineau Y00aEffects of anti-endothelial cell antibodies in leprosy and malaria.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC344010/pdf/1219.pdf  a301-90 v72  aDUGUE 20043 a<p>As a result of damaging endothelial cells (ECs), Mycobacterium leprae triggers the production of antibodies (Abs). These anti-EC Abs (AECAs) can be divided into two types. The first type nonspecifically reacts with components of the cytosol (CY) and can be detected by enzyme-linked immunosorbent assay (ELISA). The second specifically reacts with the EC membrane (MB) and requires fluorescence-activated cell sorter (FACS) analysis to be detected. The presence of both types of AECAs was determined in 68 leprosy patients. The ELISA was positive for 35 of them but also for 30 of 34 malaria patients and 17 of 50 healthy African controls. However, whereas FACS analysis showed MB reactivity in only three malaria patients and four controls, this reactivity was found in 27 leprosy patients, more of those having the lepromatous than the tuberculoid form. Specificity for MB, which we failed to absorb by incubation with CY lysates, predominated over that for CY in leprosy, unlike malaria, where the EC reactivity was restricted to the CY. Western blot analysis and two-dimensional electrophoresis revealed that calreticulin, vimentin, tubulin, and heat shock protein 70 were targeted by AECAs from leprosy patients, but other proteins remained unidentified. These auto-Abs, but not those from malaria patients, did activate ECs, as indicated by the E-selectin and intercellular adhesion molecule 1 upregulation, and/or induced them into apoptosis, as documented by four different methods. Our findings suggest that, in some but not all leprosy patients, AECAs may play a role in pathogenesis.</p>  a0019-9567