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Objectives ‐ The aim of this study was to investigate whether adhesion molecules play a role in acute ischemic stroke. Material and methods ‐Using immunofluorescence phenotyping and flow cytometry, the expression of leukocyte adhesion molecules CD54, CD11a, CD11b and CD18 in peripheral blood were measured within 12 h after onset of ischemia in 20 patients with stroke. Follow‐up measurements were performed at 7 and 30 days after ictus.Results ‐ CD 18 immunofluorescence was significantly increased on the leukocytes within 12 h after onset in patients with stroke compared with the age‐matched control group (20 patients with other neurological diseases). Follow‐up measurement of CD18 revealed normal results as found in the control group. Conclusion ‐ Our data support the idea that adhesion molecules are involved in tissue injury in ischemic stroke.

We studied the distribution of T, T helper (TH), and T suppressor (TS) cells in blood and CSF using an immunoperoxidase slide assay and monoclonal antibodies. In subacute sclerosing panencephalitis, we found an elevated level of TS and a decreased level of TH cells in both CSF and blood. In MS, the TH/TS ratio was increased.

Multiple sclerosis (MS) is a central nervous disease thought to be elicited by an autoimmune process. Many studies in recent years have concentrated on finding the alterations in the peripheral blood immune profile in MS patients that would reflect disease activity. In the present study, we investigated surface antigen expression on lymphocytes and granulocytes from MS patients and control subjects. We have studied 29 patients suffering from relapsing-remitting or relapsing-progressive forms of MS. The disease was diagnosed in all patients at least 12 months before inclusion into the study. All patients had no attack at the study entry date or within a previous month. The control group included 29 age-matched subjects. Phenotyping of peripheral blood leukocytes was carried out with different fluorescence-conjugated murine monoclonal antibodies. The analysis was performed with three-color flow cytometry. The following antigens were determined [cluster of definition (CD)]: leukocyte common antigen (LCA) (B220, T 200, Ly-5), CD45; LPS-R (lipopolysaccharide receptor), CD14; found on all T cells, CD3; LFA-2 (lymphocyte function associated antigen, T 11), CD2; coreceptor for MHC class II molecules, found on helper T cells, CD4; coreceptor for MHC class I molecules, found on suppressor/cytotoxic T cells, CD8; B4, found on all human B cells, CD19; NCAM (neural cell adhesion molecule), CD56; integrin beta2 subunit, associated with CD11a (CD11a/CD18, LFA-1, alphaLbeta2) and CD11b (CD11b/CD18, Mac-1,CR3, alphaMbeta2), CD18; alphaL, alpha subunit of integrin LFA-1 (alphaLbeta2, CD11a/CD18), CD11a; alphaM, alpha subunit of integrin Mac-1 (CR3, alphaMbeta2, CD11b/CD18), CD11b; ICAM-1 (intercellular adhesion molecule), CD54; H-CAM, Hermes antigen, Pgp-1, CD44; AIM (activation inducer molecule), early activation antigen, CD69; T-cell receptor gammadelta, TCR gammadelta. In the MS group, we have found a significant increased expression of CD54 and CD44 antigens on lymphocytes, and higher percentage CD54(+) and CD11a+CD54(+) lymphocytes out of all lymphocytes compared with the control group. We have also found a significant increased expression of CD11a, CD18 and CD54 antigens on granulocytes, and higher percentage CD11b+CD18(+) granulocytes out of all granulocytes in MS patients compared with control. Higher levels of expression of the adhesion molecules may reflect the activation state of leukocytes in MS patients.