Expression of Fractalkine receptor (CX3CR1) in monocytes (Mo) and Natural Killer (NK) cells from hemolytic uremic syndrome (HUS) patients

RAMOS M; FERNANDEZ G; SCHIERLOH P; ELIAS-COSTA C; VALLEJO G; EXENI R; ALDUNCIN M; PROULX F; SASIAIN MC; PALERMO MS

Córdoba. Argentina

Congreso; VII Latin American Congress of Immunology; 2005

Asociación Latinoamericana de Inmunología (ALAI)

Endothelial activation is central in the development of HUS, a disease caused by Stx-producing E.coli. Different subpopulations of NK and Mo express CX3CR1, the receptor for the endothelial transmembrane chemokine fractalkine, which is involved in adhesion and migration across endothelium. We investigated whether the expression of CX3CR1 is modulated in distinct whole blood populations. The expression of CX3CR1 in convination with CD62L on Mo and with CD56 on NK was determined on whole blood from HUS patients in the acute period and healthy children (HC) by flow cytometry. We found that the percentage of CX3R1+ cells was decreased in HUS compared with HC (% CX3CR1-/CD62L+: HUS= 46.6±6*, HC=26.4±5.4; % CX3CR1+/CD62L+: HUS=38.5±5.6*, HC= 59.0±6.3; % CX3CR1-/CD62L-: HUS=10.8±1.9*, HC=3.9±0.9, *p<0.05). When we analyzed NK population we found  a decreased percentage of NK cells in HUS patients (HC=14.23±1.63, HUS=3.92+0.84***, *** p<0.0001). Moreover, differences were found in subpopulations of NK cells that coexist in circulation: CD56bright/CX3CR1- and CD56dim/CXCR1+ cells (%CD56bright/CX3CR1-: HC=0.45±0.05, HUS=0.3±0.86*; CD56dim/CXCR1+: HC= 12±1.69, HUS=1.98±0.56***, ***p<0.0001; *p<0.05). A common feature of decreased CX3CR1+ leukocytes (Mo and NK) is observed in HUS patients. Possible explanations include down modulation or lost of CX3CR1, and/or activation of endothelium during HUS-associated inflammation that may adhere/retain CX3CR1+ cells.