Compartmentalization of dendritic cell and T‐cell interactions in the lymph node: Anatomy of T‐cell fate decisions

Abstract

Upon receiving cognate and co-stimulatory priming signals from antigen (Ag)-presenting dendritic cells (DCs) in secondary lymphoid tissues, naïve CD4 + T cells differentiate into distinct effector and memory populations. These alternate cell fate decisions, which ultimately control the T cell functional attributes, are dictated by programming signals provided by Ag-bearing DCs and by other cells that are present in the microenvironment in which T cell priming occurs. We know that DCs can be subdivided into multiple populations and that the various DC subsets exhibit differential capacities to initiate development of the different CD4 + T-helper populations. What is less well understood is why different sub-anatomic regions of secondary lymphoid tissues are colonized by distinct populations of Ag-presenting DCs and how the location of these DCs influences the type of T cell response that will be generated. Here we review how chemokine receptors and their ligands, which position allergen and nematode-activated DCs within different microdomains of secondary lymphoid tissues, contribute to the establishment of IL-4 committed follicular helper T (Tfh) and type 2 helper (Th2) cell responses.

Dermal IRF4+ dendritic cells and monocytes license CD4+ T helper cells to distinct cytokine profiles

“…2d ). The comparable upregulation of CCR7 suggests similar localization of Ag+ migDC2 within the dLN (reviewed in 26 ).

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Human Intestinal Mononuclear Phagocytes in Health and Inflammatory Bowel Disease

“…Unfortunately, the human cDC1 subset is rare in blood and tissues (135), making it difficult to study them ex vivo. Thus, the division of labor between cDC1 and cDC2 subsets is still not fully understood (158), but their physical location in the LNs could contribute to differences in T cell activation, as recently reviewed (159,160).…”

Dendritic Cells (DCs) as “Fire Accelerants” of Hantaviral Pathogenesis

“…In fact, DCs are equipped with numerous different pattern recognition receptors (PRRs) that act as sensors of pathogen-associated molecular patterns (PAMPs) [25]. Upon receiving signals via PRRs, migratory cDCs acquire a mature phenotype with high levels of major histocompatibility complex (MHC) class II molecules and co-stimulatory molecules on the cell surface [26]. After migration to the draining lymph nodes, mature cDCs present antigen to CD4+ and CD8+ T lymphocytes, thereby initiating powerful adaptive immune responses.…”

“…Subsequent immunohistochemical testing of tissues from patients that died of SNF infection revealed hantaviral antigen in follicular dendritic cells (FDCs) and macrophages [33]. FDCs are localized in follicles of the B-cell zone of lymphoid tissue [26] but are not related to leucocyte DCs, although they can retain antigen and virions for a long time [34]. The permissivity of DCs for Old World hantaviruses was first demonstrated in vitro by infecting DCs from various sources (monocyte-derived DCs, DCs derived from CD34+ progenitor cells) with HTNV [35].…”