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SP0035 Inflammation-induced formation of fat associated lymphoid clusters
  1. J. Caamano,
  2. on behalf of Stroma-Immune Cell Interaction Group
  1. Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences – University of Birmingham, Birmingham, UK


Fat-associated lymphoid clusters (FALCs) are atypical lymphoid tissues located on adipose tissues in mucosal surfaces such as the mesenteries, omentum, mediastinum, pericardium, and gonadal fat in humans and mice. FALCs were originally identified in mouse and human mesenteries due to that they contain a high number of type 2 innate lymphoid cells (ILC). Our work has shown that FALCs contain B1, B2 and T lymphocytes as well as myeloid and other innate immune cell populations.1,2 Inflammation induces the rapid formation of FALCs and significant changes in cellular composition. Immunizations have shown the development of adaptive immune responses including B cells undergoing a germinal centre reaction in mesenteric FALCs emphasising their function on local immunity.

Our recent results show that helminth o bacterial infections induce a significant increase in proliferation of ILC in FALCs and a massive expansion in the number of clusters at early time points. A recent report has demonstrated that mesenteric FALCs act as a reservoir of CD8 +T resident memory cells (Trm) that have been generated following infections with bacteria or parasites.3

Our current working model is that FALCs have a dual role during immune responses. At the initial stages of infection or inflammation FALCs support the activation and proliferation of innate lymphoid cells. At later stages FALCs act as reservoirs of tissue resident memory T cells through their stromal cell expression of survival factors and their association with adipocytes to support Trm metabolism and survival. Understanding what signals and cells are essential to FALC formation in homeostasis and following inflammation or infection will allow the development of therapies to reduce or prevent FALC formation during chronic inflammation and autoimmune diseases.

Reference [1] Benezech C, et al. Nat Immunol2015;16:819.3.

[2] Cruz-Migoniet al. Front. Immunol2016.

[3] Hanet al. Immunity 2017;47:1154.

Disclosure of Interest None declared

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