Systemic lupus erythematosus (SLE) is a complex and challenging disorder. At present, abnormal T cells are considered to be the key point in the pathogenesis of SLE, including the losing central immune tolerance of self-reactive T cells in the thymus, breaking of regulatory T cell balances, and the overactivation of pro-inflammatory T cells. The alterations of T-cell receptor proteins are closely related to these abnormal changes. Glycosylation is one of the most ubiquitous steps of protein post-translational modification. Especially the modifications of N-glycans and O-glycans on T-cell surfaces have been found to regulate apoptosis and downstream signalling in SLE. Accordingly, this review summarises the aberrant modulate effects of T cell glycosylation in SLE and provides new insights into understanding the pathogenesis and some potential therapeutic targets of this chronic autoimmune disease.