CD49d Is Upregulated in Circulating T Lymphocytes from HTLV-1-Infected Patients

• Published in: Neuroimmunomodulation Vol. 27; no. 2; p. 113
• Main Authors: Janahú, L T Araújo, Da Costa, Carlos Araujo, Vallinoto, Antonio Carlos Rosário, Santana, Barbara Brasil, Ribeiro-Lima, Jessica, Santos-Oliveira, Joanna Reis, Chometon, Thaize Quiroga, Bertho, Alvaro Luis, Savino, Wilson, Da-Cruz, Alda Maria, Gomes-Silva, Adriano
• Format: Journal Article
• Language: English
• Published: Switzerland 2020
• Subjects: T lymphocytes; VLA-4 (CD49d); HTLV-1; Cytokines; Integrins
• ISSN: 1423-0216
• DOI: 10.1159/000507086

HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a chronic progressive myelopathy associated with an inflammation of the central nervous system (CNS), being characterized by perivascular infiltration of inflammatory cells. HTLV-1-infected cells have the capacity to migrate through endothelial layers by enhancing adhesion receptor expression and corresponding ligands. T cells interact with the extracellular matrix via integrin receptors and these interactions affect both cell migration and proliferation. The importance of these interactions in retrovirus-induced diseases, however, remains less clear. Herein we studied the expression of 3 integrin alpha chains (CD49d, CD49e, and CD49f) on the membrane of T-cell subsets in patients infected by HTLV-1, both HAM/TSP patients and oligo/asymptomatic subjects who were asymptomatic or presented slight manifestations related to the virus infection. We observed higher peripheral blood frequency of CD49dhiCD4+ and CD49dhiCD8+ T cells in HTLV-1-infected patients. Our findings suggest that the increased expression of adhesion molecules, such as CD49d on T lymphocytes from HTLV-1-infected patients may contribute to the pathogenesis of the disease, in both oligo/asymptomatic and HAM/TSP-infected subjects. Accordingly, it is conceivable that there is a potential use of CD49d as target for a therapeutic approach aiming at blocking migration of activated T cells from HTLV-1-infected patients into the CNS, thus avoiding the progression to HAM/TSP.