Abstract
Follicular dendritic cells (FDCs) are stromal cells residing in primary follicles and in germinal centers of secondary and tertiary lymphoid organs (SLOs and TLOs). There, they play a crucial role in B-cell activation and affinity maturation of antibodies. FDCs have the unique capacity to bind and retain native antigen in B-cell follicles for long periods of time. Therefore, FDCs shape the B-cell antigenome (the sum of all B-cell antigens) in SLOs and TLOs. In this review, we discuss recent findings that explain how this stromal cell type can arise in almost any tissue during TLO formation and, furthermore, focus on the mechanisms of antigen capture and retention involved in the generation of long-lasting antigen depots displayed on FDCs.
Highlights
Specialty section: This article was submitted to Inflammation, a section of the journal Frontiers in Immunology
We think it is important to understand what the consequences of such antigen storage are for the activation of B cells, especially during chronic inflammations, where Follicular dendritic cells (FDCs)-containing tertiary lymphoid organ (TLO) arise in non-lymphoid tissues, e.g., during rheumatoid arthritis [85]
Little is known, how antigen is acquired by FDCs in TLOs, it might differ from antigen acquisition in lymph nodes or spleen
Summary
After the first mentioning of FDCs little more than half a decade ago, initial experiments, mainly using bone marrow chimeras [6, 7], indicated that FDCs are of stromal, radioresistant, and likely sessile character. In parabiont experiments, where the blood circulation of two mice was surgically connected for 3 months, no FDCs had been generated from the surgically attached counterpart [24] This corroborated a model of a non-migratory and rather local precursor, giving rise to FDCs. In a murine model of chronic inflammation, transgenic overexpression of LTα under the rat insulin promoter (RIPLta) leads to the formation of TLOs in kidneys, including fully matured FDCs [25,26,27]. FDCs, MRCs, and FRCs share the expression of many markers, such as LTβR, BP-3, VCAM-1, and ICAM-1 [25, 33,34,35], which could suggest a common precursor To identify this potential precursor, labeling experiments were performed with fetal mesenchymal progenitors of spleen and lymph nodes.
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