Factors supporting intrathecal humoral responses following viral XXXX .

@entity4767 @entity6220 @entity404 @entity39 @entity5 @entity405 @entity281 @entity15787 @entity379 @entity373 @entity1651 @entity371 @entity366 @entity792 @entity372
@entity4767 and @entity792 are often associated with retention of antibody-secreting cells (ASC). Although beneficial or detrimental contributions of ASC to @entity6220 remain to be defined, virus-specific ASC are crucial in controlling persistent CNS @entity281 following coronavirus-induced @entity1651 . This report characterizes expression kinetics of factors associated with ASC homing, differentiation, and survival in the spinal cord, the prominent site of coronavirus persistence. Infection induced a vast, @entity379 )-dependent, prolonged increase in @entity373 ( @entity373 ), @entity371 , and @entity372 mRNA, supporting a role for @entity373 (C @entity366 -mediated ASC recruitment. Similarly, C @entity404 T cell-secreted i @entity15787 a critical regulator of both peripheral activated B cells and C @entity405 T cells, was sustained during viral persistence. The ASC survival factors B cell-activating factor of the t @entity5 n @entity39 factor (TNF) family (BAFF) and a proliferating-inducing ligand (APRIL) were also significantly elevated in the infected CNS, albeit delayed relative to the chemokines. Unlike IFN-y-dependent BAFF upregulation, APRIL induction was IFN-y independent. Moreover, both APRIL and BAFF were predominantly localized to astrocytes. Last, the expression kinetics of the APRIL and BAFF receptors coincided with CNS accumulation of ASC. Therefore, the factors associated with ASC migration, differentiation, and survival are all induced during acute viral e @entity1651 prior to ASC accumulation in the CNS. Importantly, the CNS expression kinetics implicate rapid establishment, and subsequent maintenance, of an environment capable of supporting differentiation and survival of protective antiviral ASC, recruited as plasmablasts from lymphoid organs.
