![]() IMPORTANCE The prevalence and role of antigen-specific Bmem in the CNS during viral encephalomyelitis is largely undefined. Ongoing GC reactions and regional signals further regulate dynamics within the CNS, with preferential maintenance of tdTomato + B cells in spinal cords relative to that in brains during viral persistence. Overall, the data support the idea that virus-induced B cells exhibiting SHM require peripheral GC formation to emerge in the CNS. Delayed tamoxifen treatment demonstrated ongoing CNS recruitment of tdTomato + B cells, mainly ASC, primed late during GC reactions. While they initially comprised mainly Bmem, the proportions of ASC and Bmem became similar as tdTomato + B cells increased throughout viral persistence. In the CNS, tdTomato + cells started emerging at day 14 p.i. Moreover, their proportion of Bmem dominated over the proportion of ASC throughout infection. ![]() In draining lymph nodes, tdTomato-positive (tdTomato +) ASC were most prevalent prior to germinal center (GC) formation, but total tdTomato + B cells only peaked with robust GC formation at day 14 p.i. AID detection via tdTomato expression allowed tracking of virus-specific ASC and Bmem in priming and effector sites throughout infection. This study takes advantage of the progeny of mice expressing tamoxifen-inducible Cre recombinase (Cre-ERT2) under the Aicda promoter crossed with Rosa26-loxP-tdTomato reporter mice (AID Cre-Rosa26 tdTomato) to monitor B cells having undergone activation-induced cytidine deaminase (AID)-mediated somatic hypermutation (SHM) following neurotropic coronavirus infection. However, a role for virus-specific memory B cells (Bmem) within the CNS is poorly explored due to lack of robust phenotypic or functional identification in mice. ![]() Humoral responses within the central nervous system (CNS) are common to many neurotropic viral infections, with antibody (Ab)-secreting cells (ASC) contributing to local protection. ![]()
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