The following is a summary of “Aberrant follicular regulatory T cells associate with immunoglobulin hyperproduction in nasal polyps with ectopic lymphoid tissues,” published in the April 2024 issue of Allergy & Immunology by Song, et al.
Ectopic lymphoid tissues (eLTs) and follicular helper T (TFH) cells play a role in local immunoglobulin hyperproduction in nasal polyps (NPs). While follicular regulatory T (TFR) cells in secondary lymphoid organs counteract TFH cells, their presence and function in eLTs in peripheral diseased tissues were not well understood. For a study, researchers sought to investigate the presence, phenotype, and function of TFR cells in NPs.
Various techniques, including single-cell RNA sequencing, immunofluorescence staining, and flow cytometry, were employed to examine the presence, abundance, and phenotype of TFR cells in NPs. Coculture experiments with sorted polyp and circulating T-cell subsets were conducted with autologous circulating naïve B cells to assess cytokine and immunoglobulin production.
TFR cells were primarily localized within eLTs in NPs, with their frequency and TFR cell/TFH cell ratio decreased in NPs with eLTs compared to those without and control inferior turbinate tissues. TFR cells in NPs exhibited a phenotype similar to TFH cells and FOXP3+ regulatory T cells. Polyp TFR cells showed reduced CTLA-4 expression and diminished capacity to inhibit TFH cell-induced immunoglobulin production compared to their counterparts in blood and tonsils. Blocking CTLA-4 abolished the suppressive effect of TFR cells. Moreover, polyp TFR cells displayed lower vitamin D receptor expression, which correlated with impaired suppressive function. Treatment with vitamin D upregulated CTLA-4 expression on polyp TFR cells and restored their suppressive function in vitro.
TFR cells in eLTs of NPs exhibit decreased CTLA-4 and vitamin D receptor expression, leading to impaired suppression of TFH cell-induced immunoglobulin production. However, vitamin D treatment can reverse this phenotype in vitro, suggesting a potential therapeutic approach for NP-associated immunoglobulin hyperproduction.
Reference: sciencedirect.com/science/article/abs/pii/S0091674923024107