Expression of aminopeptidase N (APN) on peripheral blood mononuclear cells' surface as a marker of these cells' transendothelial migration properties in the course of multiple sclerosis.

CD13 Ag and CD11a, CD11b, CD18 molecule expression on peripheral blood mononuclear cells (PBMC) were studied as these cells' adherent or transendothelial migration properties in three different multiple sclerosis (MS) patients groups (total 38): with clinically active MS (acute exacerbation of MS and primary chronic progressive MS (CP-MS)) and with MS remission. The control group consisted of patients, suffering from other non-inflammatory neurological diseases (OND). The results of our study suggest that CD11a/CD18 molecules expression on PB lymphocytes, although higher on these cells' surface in the course of MS as compared to OND, does not differentiate clinical forms of MS. CD11a molecule expression on monocytes did not differ significantly in all tested MS patient groups in comparison to OND. Although the expression of CD11b/CD18 molecules on monocytes' surface shows their activation in the course of MS, it does not differentiate them either. However, CD13 Ag of APN expression on PBMC surface may be an immunological marker of MS clinical form. CD13 Ag expression may also be a sensitive marker of these cells' transendothelial migration properties

The immunoregulatory abilities of polymorphonuclear neutrophils in the course of multiple sclerosis.

The polymorphonuclear neutrophils (PMN) possess sufficient potential to affect both immune response and inflammation, however it has not been yet described in the course of multiple sclerosis (MS). We have studied binding of fluorescein isothiocyanate (FITC)- stained TNF-alpha by PMN, the expression of CD11a, CD11b, and CD18 molecules of beta2-integrines and the expression of CD10 (neutral endopeptidase-NEP) and of CD13 (aminopeptidase N; APN) antigens on PMN in three different groups of MS patients. The control group included neurological patients (OND) with noninflammatory diseases. The obtained results have proved that during MS exacerbation and in the course of chronic progressive MS, PMN reveal several forms of preactivation, including significantly higher stained-TNF-alpha binding, higher expression of CD11b and CD18, as well as CD10 and CD13 antigens, in comparison with MS remission or OND. We suggest that the increased expression of these molecules on PMN of MS patients in exacerbation of the disease and to a lower degree in the course of CP-MS is a result of PMN priming, and directly prove the PMN involvement in the disease pathogenesis