Chronic type I IFN production in SLE shifts the differentiation of naïve CD4+ T cells from a Th1 effector subset toward a dominant T follicular helper cell phenotype, promoting B cell differentiation, immunoglobulin class switching, affinity maturation and ultimately leading to the secretion of antinuclear antibodies (ANAs), which are an immunological hallmark of SLE [26,27]. Here, CD4 is linked to systemic lupus erythematosus.