Lung-resident CD4~+ T cells are sufficient for IL-4Rα-dependent recall immunity to Nippostrongylus brasiliensis infection

摘要

Immunity to Nippostrongylus brasiliensis reinfection requires pulmonary CD4~+ T-cell responses.We examined whether secondary lymphoid recruited or pre-existing lung CD4~+ T-cell populations coordinated this immunity. To do this, we blocked T-cell egress from lymph nodes using Fingolimod (FTY720). This impaired host ability to resolve a primary infection but did not change effectiveness of recall immunity. Associated with this effective recall immunity was the expansion and T helper type 2 polarization of a pre-existing pulmonary CD4~+ T-cell population. LTbR-Ig (lymphotoxin beta-receptor fusion protein)-mediated disruption of stromal cell organization of immune cells did not disrupt this recall immunity, suggesting that protection was mediated by a pulmonary interstitial residing CD4~+ T-cell population. Adoptive transfer of N. brasiliensis-experienced pulmonary CD4~+ T cells from FTY720-treated wild-type or T-cell interleukin (IL)-4Ra-deficient mice demonstrated protection to be IL-4Ra dependent. These results show that preexisting CD4~+ Tcells can drive effective recall immunity to N. brasiliensis infection independently of T-cell recruitment from secondary lymphoid organs.