Investigation of integrins expressed on T helper cell surfaces during relapsing and remitting phases in patients with (relapsing/remitting) multiple sclerosis

Objective: Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system. The etiology of the disease still remains unclear. It is thought that one of the underlying mechanisms involves excessively activated T helper lymphocytes migrating from the peripheral blood across the blood–brain barrier and secreting inflammatory cytokines within the central nervous system. This study was designed to investigate whether the changes occurring in T helper lymphocyte subsets during the attack phase of patients with relapsing–remitting multiple sclerosis (RR-MS) can be identified through peripheral blood analysis. For this purpose, the proportions of Treg, Th1, Th2, Th17, and Th17.1 cells, as well as the proportions of T helper lymphocytes expressing the cell-surface integrins αLβ2, αMβ2, α4, and β3 which are considered to play a role in crossing the blood–brain barrier and initiating inflammation were determined in the peripheral blood of RR-MS patients during attack and remission phases. Materials and Methods: Our study was designed as a prospective investigation, and it included 20 patients with relapsing–remitting multiple sclerosis (RR-MS) in the attack phase and 20 patients in the remission phase who presented to the Department of Neurology at Afyonkarahisar University of Health Sciences, Faculty of Medicine Hospital. In addition, 20 healthy individuals without any known acute or chronic disease were enrolled as controls. Peripheral venous blood samples were obtained from all participants, and T helper lymphocyte proportions and integrin expression levels were determined using flow cytometry. Statistical comparisons were then performed among the control, attack, and remission groups. Result: When the mean ± SD values were examined across the three groups, the total lymphocyte level was lower in the attack group (25.73% ± 7.35) compared with the control group (33.05% ± 8.74) (p = 0.007). The Th cell level was higher in the remission group (49.30% ± 9.09) than in the control group (42.85% ± 6.22) (p = 0.038). The Th17.1 cell level was found to be higher in the attack group (17.47% ± 3.06) compared with the control group (14.16% ± 3.24) (p = 0.042). In addition, the Th2/Th17 ratio was lower in the attack group (2.16 ± 0.53) than in the control group (3.41 ± 1.02). The αMβ2 expression level on Th17.1 cells was lower in both the attack group (1.36% ± 0.80) and the remission group (1.47% ± 1.15) compared with the control group (2.55% ± 1.50) (p <0.05). The α4 expression level on Th1 cells was also lower in the attack group (77.56% ± 8.68) than in the control group (83.48% ± 4.78) (p = 0.027). Conclusion: The detection of elevated Th17.1 cell levels in the peripheral blood of the attack group in this study along with the observation that the Th2/Th17.1 ratio was lower in the attack group suggests that the Th17.1 subset may serve as a practical indicator of the attack phase in multiple sclerosis, a cell population increasingly recognized for its important role in MS pathogenesis. We concluded that integrin expression levels on peripheral T helper lymphocytes are not suitable markers for distinguishing the attack phase.