Accelerated immune aging was correlated with lupus-associated brain fog in reproductive-age systemic lupus erythematosus patients

Aims Cognitive impairment is common in systemic lupus erythematosus (SLE) patients with substantial adverse effects on function and quality of life. One hypothesis to understand the mechanisms of cognitive impairment in SLE is accelerated immunosenescence. The aim of this study is to observe the correlation between immunosenescence with cognitive impairment in patients with SLE. Methods Sixty-one female SLE patient were measured for CD4 and CD8 T cell-associated senescence markers, including percentage of end-stage differentiated T cells (CD4 and CD8 T cells expressing CD57(+) or loss of CD28 expression), of naive T cells (CD4(+)CD45RA(+) and CD8(+)CD45RA(+)), memory T cells (CD4(+)CD45RO(+) and CD8(+)CD45RO(+)), and antigen-experienced T cells (CD4(+)KLRG1(+) and CD8(+)KLRG1(+)) which were measured using flow cytometry. One hallmark of immunosenescence called immune risk profile (IRP) was defined by an inverted ratio of CD4 and CD8. Cognitive functions were measured by Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MOCA) questionnaire. Results Thirty-six (59.1%) SLE patients who had IRP develop significantly lower attention and recall from both MMSE (P = .005 and P = .000) and MOCA (P = .017 and P = .000) examinations. Decreased visuospatial ability was also found in patients with IRP measured by MOCA (P = .046). There was a negative correlation between memory CD4(+)CD45RO(+) T cells with recall and visuospatial domain (R = -0.204, P = .039 and R = -0.250, P = .033; respectively), and negative correlation between CD8(+)CD28(-) T cells with recall and attention domain (R = -0.249, P = .027 and R = -0.145, P = .048, respectively). Conclusion Systemic lupus erythematosus patients develop an accelerated immunosenescence which contributes to cognitive dysfunction, especially in attention, recall, and visuospatial domains.