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Journal articles on the topic 'Organe lymphoïde tertiaire'

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Published: 7 December 2024

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1

Shomer, Nirah H., James G. Fox, Amy E. Juedes, and Nancy H. Ruddle. "Helicobacter-Induced Chronic Active Lymphoid Aggregates Have Characteristics of Tertiary Lymphoid Tissue." Infection and Immunity 71, no. 6 (June 2003): 3572–77. http://dx.doi.org/10.1128/iai.71.6.3572-3577.2003.

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ABSTRACT Susceptible strains of mice that are naturally or experimentally infected with murine intestinal helicobacter species develop hepatic inflammatory lesions that have previously been described as chronic active hepatitis. The inflammatory infiltrates in some models of chronic autoimmunity or inflammation resemble tertiary lymphoid organs hypothesized to arise by a process termed lymphoid organ neogenesis. To determine whether hepatic inflammation caused by infection with helicobacter could give rise to tertiary lymphoid organs, we used fluorescence-activated cell sorting, immunohistochemistry, and in situ hybridization techniques to identify specific components characteristic of lymphoid organs in liver tissue sections and liver cell suspensions from helicobacter-infected mice. Small venules (high endothelial venules [HEVs]) in inflammatory lesions in Helicobacter species-infected livers were positive for peripheral node addressin. Mucosal addressin cell adhesion molecule also stained HEVs and cells with a staining pattern consistent with scattered stromal cells. The chemokines SLC (CCL 21) and BLC (CXCL13) were present, as were B220-positive B cells and T cells. The latter included a naïve (CD45lo-CD62Lhi) population. These findings suggest that helicobacter-induced chronic active hepatitis arises through the process of lymphoid organ neogenesis.

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2

Barone, Francesca, Saba Nayar, Joana Campos, Thomas Cloake, David R. Withers, Kai-Michael Toellner, Yang Zhang, et al. "IL-22 regulates lymphoid chemokine production and assembly of tertiary lymphoid organs." Proceedings of the National Academy of Sciences 112, no. 35 (August 18, 2015): 11024–29. http://dx.doi.org/10.1073/pnas.1503315112.

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The series of events leading to tertiary lymphoid organ (TLO) formation in mucosal organs following tissue damage remain unclear. Using a virus-induced model of autoantibody formation in the salivary glands of adult mice, we demonstrate that IL-22 provides a mechanistic link between mucosal infection, B-cell recruitment, and humoral autoimmunity. IL-22 receptor engagement is necessary and sufficient to promote differential expression of chemokine (C-X-C motif) ligand 12 and chemokine (C-X-C motif) ligand 13 in epithelial and fibroblastic stromal cells that, in turn, is pivotal for B-cell recruitment and organization of the TLOs. Accordingly, genetic and therapeutic blockade of IL-22 impairs and reverses TLO formation and autoantibody production. Our work highlights a critical role for IL-22 in TLO-induced pathology and provides a rationale for the use of IL-22–blocking agents in B-cell–mediated autoimmune conditions.

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3

Erlich, Emma, Rafael Czepielewski, Shashi Kumar, Rachael Field, Xinya Zhang, Leila Saleh, Farshid Guilak, Jonathan Brestoff, Ali Ellebedy, and Gwendalyn J. Randolph. "B cells drive tertiary lymphoid organ formation in ileal inflammation." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 113.18. http://dx.doi.org/10.4049/jimmunol.208.supp.113.18.

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Abstract Crohn’s disease [CD] is one of the two most common forms of inflammatory bowel disease, affecting over half a million Americans. Like many other diseases with chronic inflammation, some patients with CD develop tertiary lymphoid organs [TLO] in areas of the gastrointestinal tract with active disease. TLOs are organized clusters of lymphocytes, similar in structure to secondary lymphoid organs, though they develop after birth and their contribution to pathogenesis in CD, or other diseases, is unclear. We, and others, have also found B cell rich lymphoid aggregates in the mesenteric fat of CD patients along dramatically remodeled lymphatic vessels. TNFΔARE/+ is a murine model of ileal inflammation that recapitulates several key features of ileal CD, including development of mesenteric tertiary lymphoid organs. Use of this model revealed that mesenteric TLOs block cellular and molecular export from the gut, leading us to wonder if mechanisms that interfere with their development might reduce ileitis. TNFΔARE/+ mice that lack B cells revealed that B cells are required for tertiary lymphoid organ formation in this model. Without these TLOs, lymphatic outflow from the intestine was restored. Nonetheless, histological and flow cytometric approaches reveal no difference in local inflammation in the ileum. However, systemic inflammation, as assessed by metabolic cages and changes in body weight over time, increased. This suggests that TLOs may act to trap inflammatory signals locally, preventing systemic dissemination of inflammatory cells or mediators. Work supported by NIH grants DP1-DK109668-04 and T32-DK077653-27 and the Kenneth Rainin Foundation

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4

Ruddle, Nancy H. "Lymphatic vessels and tertiary lymphoid organs." Journal of Clinical Investigation 124, no. 3 (March 3, 2014): 953–59. http://dx.doi.org/10.1172/jci71611.

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5

Kirsh, Andrew L., Sharon L. Cushing, Eunice Y. Chen, Stephen M. Schwartz, and Jonathan A. Perkins. "Tertiary Lymphoid Organs in Lymphatic Malformations." Lymphatic Research and Biology 9, no. 2 (June 2011): 85–92. http://dx.doi.org/10.1089/lrb.2010.0018.

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6

Feizi, Neda, Neda Feizi, Gang Zhang, Latha Halesha, Khodor Abou Daya, and Martin H. Oberbarnscheidt. "Tertiary Lymphoid Organs promote allograft rejection." Journal of Immunology 212, no. 1_Supplement (May 1, 2024): 0321_5062. http://dx.doi.org/10.4049/jimmunol.212.supp.0321.5062.

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Abstract Tertiary lymphoid organs (TLOs) are ectopic lymphoid structures that arise in non-lymphoid tissues and are frequently observed in tissue affected by non-resolving chronic inflammation. If TLOs are beneficial or detrimental in transplantation is controversial. We investigate the role of TLO and LTbR in transplantation by manipulating the LTa-LTbR pathway. Using a mouse allo kidney transplantation model, we found that preformed intragraft TLO are sufficient to precipitate rejection in recipients lacking all secondary lymphoid organs (SLO)(LTbRko). In WT recipients with a complete set of SLO, intragraft TLO accelerated rejection (MST=63 vs. 225 d). Donor grafts that cannot form TLO (LTbRko) prolonged allograft survival (MST 24 vs 11 d) in an acute kidney rejection model. Intravital imaging confirmed that T and B cell activation takes place in renal TLO upon migration of naïve T and B cells and prolonged interactions with dendritic cells. T cells produced IFNg and Confetti+/+ B cells clonally expanded within TLO. In summary, intragraft TLO are sufficient for and accelerate allograft rejection. Local immune responses are initiated and maintained in intragraft TLO, while disruption of TLO formation in the allograft leads to prolonged allograft survival. TLO support T and B cell activation as well as local DSA formation. These findings highlight the importance of TLO in local immune responses with implications for cancer, autoimmunity and transplantation.

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7

Goyal, Girija, Lucas Barck, Yunhao Zhai, Pranav Prabhala, Sudip Paudel, Min Wen Ku, Aditya Patil, Abdul Isaacs, and Donald Ingber. "Human implantable tertiary lymphoid organs (TLO) for solid tumor therapy: from organ chips to the clinic?" Journal of Immunology 212, no. 1_Supplement (May 1, 2024): 0731_7312. http://dx.doi.org/10.4049/jimmunol.212.supp.0731.7312.

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Abstract We previously created an in vitro human TLO model from patient-derived, circulating immune cells using organ-on-a-chip devices and 3D culture in extracellular matrix (ECM). B cells in these TLOs express activation induced cytidine deaminase, which is only expressed in lymphoid tissues and is required for class switching and somatic hypermutation (SHM). When challenged by vaccines, these TLO undergo SHM and produce antigen-specific antibodies and CD8 T cells. To model cancer associated TLOs, we integrated human pancreatic and lung cancer cell lines into these TLO Chips to understand how the immune context of hot and cold tumors differentially impacts TLO formation. The high PDL1/L2 expressing lung cancer cell line that displayed a “hot” phenotype in published murine studies induced high levels of cytokines and stimulated increased TLO formation in the lymphoid Organ Chip. In contrast, the cold, low PDL1/L2 expressing lung and pancreatic cell lines did not induce this cytokine signature or TLO formation. Importantly, TLO assembly correlated with increased B cell activation, anti-tumor CD8 activity, and tumor cell death. When the same mix of immune cells and ECM was injected in humanized mice bearing subcutaneous tumors from the hot lung cancer cell line, new lymphoid tissue containing dense aggregates of T and B cells was induced, showing for the first time that direct injection of synthetic TLOs at the tumor site may offer an alternative form of therapy for solid tumors.

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8

Lau, Aden, Susan Lester, Sophia Moraitis, Judy Ou, Alkis J. Psaltis, Shaun McColl, Maureen Rischmueller, Peter-John Wormald, and Sarah Vreugde. "Tertiary lymphoid organs in recalcitrant chronic rhinosinusitis." Journal of Allergy and Clinical Immunology 139, no. 4 (April 2017): 1371–73. http://dx.doi.org/10.1016/j.jaci.2016.08.052.

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9

Neyt, Katrijn, Frédéric Perros, Corine H. GeurtsvanKessel, Hamida Hammad, and Bart N. Lambrecht. "Tertiary lymphoid organs in infection and autoimmunity." Trends in Immunology 33, no. 6 (June 2012): 297–305. http://dx.doi.org/10.1016/j.it.2012.04.006.

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10

Shipman, William D., Dragos C. Dasoveanu, and Theresa T. Lu. "Tertiary lymphoid organs in systemic autoimmune diseases: pathogenic or protective?" F1000Research 6 (February 28, 2017): 196. http://dx.doi.org/10.12688/f1000research.10595.1.

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Tertiary lymphoid organs are found at sites of chronic inflammation in autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. These organized accumulations of T and B cells resemble secondary lymphoid organs and generate autoreactive effector cells. However, whether they contribute to disease pathogenesis or have protective functions is unclear. Here, we discuss how tertiary lymphoid organs can generate potentially pathogenic cells but may also limit the extent of the response and damage in autoimmune disease.

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11

Zhang, Xueguang, and Binfeng Lu. "IL-17 initiates tertiary lymphoid organ formation." Cellular & Molecular Immunology 9, no. 1 (December 19, 2011): 9–10. http://dx.doi.org/10.1038/cmi.2011.48.

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12

Goyal, Girija, Jaclyn Long, Oren Levy, and Donald E. Ingber. "Biologically Inspired, iterative engineering of a Human Lymphoid Follicle Chip." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 120.34. http://dx.doi.org/10.4049/jimmunol.200.supp.120.34.

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Abstract Organs Chips are microengineered, three-dimensional (3D) in vitro models that simulate organ-level pathophysiology and therapeutic responses with high fidelity. Here, we report the development of an in vitro model of lymphoid follicles seen in germinal centers and sites of chronic inflammation. The Human Lymphoid Follicle Chip was designed to mimic lymph flow through the lymph node as well as its cellular and matrix composition. A subcapsular sinus like channel allows the media to flow around the follicles with a fraction of it flowing through the parenchyma. We provide the first known evidence that 3D organization, cellular density and physical forces such as interstitial flow play a role in formation of tertiary lymphoid organs and germinal centers. Like tertiary lymphoid organs, CXCL3 production by lymphocytes is observed in the follicle chip concomitant with the aggregation of T and B cells. The follicles formed in vitro recapitulate the gross expansion and production of antibodies and cytokines seen in vivo in response to bacterial stimulation. While trying to incorporate vasculature into the follicle on chip, we found that our in vitro cultures mimic the killing of allogeneic endothelial cells, a clinically important phenotype in graft rejection that previously couldn’t be modeled without humanized mice. Mice and conventional two-dimensional (2D) cultures of circulating human immune cells, even together, can fail to replicate human biology, leading to low efficacy and unpredicted, sometimes severe toxicity in clinical trials. In future experiments, the Follicle Chip will enable the assessment of candidate therapeutics, and specifically immunotherapies, in a patient-specific manner in vitro.

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13

Clement, Marc, Kevin Guedj, Francesco Andreata, Marion Morvan, Laetitia Bey, Jamila Khallou-Laschet, Anh-Thu Gaston, et al. "Control of the T Follicular Helper–Germinal Center B-Cell Axis by CD8 + Regulatory T Cells Limits Atherosclerosis and Tertiary Lymphoid Organ Development." Circulation 131, no. 6 (February 10, 2015): 560–70. http://dx.doi.org/10.1161/circulationaha.114.010988.

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Background— The atheromodulating activity of B cells during the development of atherosclerosis is well documented, but the mechanisms by which these cells are regulated have not been investigated. Methods and Results— Here, we analyzed the contribution of Qa-1–restricted CD8 + regulatory T cells to the control of the T follicular helper–germinal center B-cell axis during atherogenesis. Genetic disruption of CD8 + regulatory T cell function in atherosclerosis-prone apolipoprotein E knockout mice resulted in overactivation of this axis in secondary lymphoid organs, led to the increased development of tertiary lymphoid organs in the aorta, and enhanced disease development. In contrast, restoring control of the T follicular helper–germinal center B-cell axis by blocking the ICOS-ICOSL pathway reduced the development of atherosclerosis and the formation of tertiary lymphoid organs. Moreover, analyses of human atherosclerotic aneurysmal arteries by flow cytometry, gene expression analysis, and immunofluorescence confirmed the presence of T follicular helper cells within tertiary lymphoid organs. Conclusions— This study is the first to demonstrate that the T follicular helper–germinal center B-cell axis is proatherogenic and that CD8 + regulatory T cells control the germinal center reaction in both secondary and tertiary lymphoid organs. Therefore, disrupting this axis represents an innovative therapeutic approach.

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14

Frija-Masson, Justine, Clémence Martin, Lucile Regard, Marie-Noëlle Lothe, Lhousseine Touqui, Aurélie Durand, Bruno Lucas, et al. "Bacteria-driven peribronchial lymphoid neogenesis in bronchiectasis and cystic fibrosis." European Respiratory Journal 49, no. 4 (April 2017): 1601873. http://dx.doi.org/10.1183/13993003.01873-2016.

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We aimed to characterise lymphoid neogenesis in bronchiectasis and cystic fibrosis (CF) lungs and to examine the role of bacterial infection.Lymphoid aggregates were examined using immunohistochemical staining and morphometric analysis in surgical lung sections obtained from nonsmokers and patients with bronchiectasis or CF. Sterile, Pseudomonas aeruginosa- or Staphylococcus aureus-coated agarose beads were instilled intratracheally in mice. Kinetics of lymphoid neogenesis and chemokine expression were examined over 14 days.Lymphoid aggregates were scarce in human lungs of nonsmokers, but numerous peribronchial lymphoid aggregates containing B-lymphocytes, T-lymphocytes, germinal centres and high endothelial venules were found in bronchiectasis and CF. Mouse lungs contained no lymphoid aggregate at baseline. During persistent P. aeruginosa or S. aureus airway infection peribronchial lymphoid neogenesis occurred. At day 14 after instillation, lymphoid aggregates expressed markers of tertiary lymphoid organs and the chemokines CXCL12 and CXCL13. The airway epithelium was an important site of CXCL12, CXCL13 and interleukin-17A expression, which began at day 1 after instillation.Peribronchial tertiary lymphoid organs are present in bronchiectasis and in CF, and persistent bacterial infection triggered peribronchial lymphoid neogenesis in mice. Peribronchial localisation of tertiary lymphoid organs and epithelial expression of chemokines suggest roles for airway epithelium in lymphoid neogenesis.

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15

Bonnan, M. "Organes lymphoïdes tertiaires méningés : des acteurs majeurs de l’auto-immunité intrathécale." Revue Neurologique 171, no. 1 (January 2015): 65–74. http://dx.doi.org/10.1016/j.neurol.2014.08.003.

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16

Daya, Khodor Abou, Daqiang Zhao, Kyle Biery, and Martin H. Oberbarnscheidt. "Tertiary lymphoid organs in renal chronic allograft rejection." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 161.14. http://dx.doi.org/10.4049/jimmunol.204.supp.161.14.

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Abstract Chronic allograft rejection remains a major obstacle to long-term allograft survival. The immunologic role of tertiary lymphoid organs (TLO) in allograft rejection is unclear. Here, we employed a chronic renal allograft rejection model in mice and intravital 2-photon microscopy to investigate the function of TLO in transplant rejection. CB6F1 (F1) RIP-LTα (preformed TLO) or F1 (no TLO) kidney grafts were transplanted to WT B6 recipients and survival monitored. To investigate immunologic function of TLO, we adoptively transferred B6-RIPLTα CD11c-YFP mice with 10m naïve dsRed OT-I T cells or 10m CTR-labeled NP-specific B cells + 10m CFP+ OT-II cells and immunized with NP-OVA + alum. Intravital 2P imaging of renal TLO was performed at time points 0, 3, 6, 24 or 72 hours after immunization. 4D image analysis was performed and mean speed, displacement, arrest coefficient (AC) and contact times (CT) with DC were calculated for OT-I, OT-II and NP-B cells. F1 RIP-LTα grafts rejected significantly faster (MST= 54) than F1 grafts (MST= 225), demonstrating that TLO contribute to allograft rejection. F1 RIP-LTα grafts contained similar numbers of, but larger TLO than F1 grafts as demonstrated by histology. Mean speed and displacement of OT-I and OT-II cells significantly decreased over time after immunization while AC and mean CT significantly increased. B cell mean speed, displacement and AC increased after immunization. These data are consistent with B cell activation and productive T cell-DC interactions and mirror previously reported data in secondary lymphoid organs. We provide first evidence that TLO provide a local structure for T and B cell activation that propagates anti-graft immune responses in the setting of chronic rejection.

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17

Maehara, Takashi, Hamid Mattoo, Vinay S. Mahajan, Samuel JH Murphy, Grace J. Yuen, Noriko Ishiguro, Miho Ohta, et al. "The expansion in lymphoid organs of IL-4+ BATF+ T follicular helper cells is linked to IgG4 class switching in vivo." Life Science Alliance 1, no. 1 (January 2018): e201800050. http://dx.doi.org/10.26508/lsa.201800050.

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Distinct T follicular helper (TFH) subsets that influence specific class-switching events are assumed to exist, but the accumulation of isotype-specific TFH subsets in secondary lymphoid organs (SLOs) and tertiary lymphoid organs has not been hitherto demonstrated. IL-4–expressing TFH cells are surprisingly sparse in human SLOs. In contrast, in IgG4-related disease (IgG4-RD), a disorder characterized by polarized Ig class switching, most TFH cells in tertiary and SLOs make IL-4. Human IL-4+ TFH cells do not express GATA-3 but express nuclear BATF, and the transcriptomes of IL-4–secreting TFH cells differ from both PD1hi TFH cells that do not secrete IL-4 and IL-4–secreting non-TFH cells. Unlike IgG4-RD, IL-4+ TFH cells are rarely found in tertiary lymphoid organs in Sjögren’s syndrome, a disorder in which IgG4 is not elevated. The proportion of CD4+IL-4+BATF+ T cells and CD4+IL-4+CXCR5+ T cells in IgG4-RD tissues correlates tightly with tissue IgG4 plasma cell numbers and plasma IgG4 levels in patients but not with the total plasma levels of other isotypes. These data describe a disease-related TFH subpopulation in human tertiary lymphoid organs and SLOs that is linked to IgG4 class switching.

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18

Akhavanpoor, Mohammadreza, Christian A. Gleissner, Hamidreza Akhavanpoor, Felix Lasitschka, Andreas O. Doesch, Hugo A. Katus, and Christian Erbel. "Adventitial tertiary lymphoid organ classification in human atherosclerosis." Cardiovascular Pathology 32 (January 2018): 8–14. http://dx.doi.org/10.1016/j.carpath.2017.08.002.

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19

Motallebzadeh, R., S. Rehakova, M. Goddard, M. Negus, E. M. Bolton, N. Ruddle, J. A. Bradley, and G. J. Pettigrew. "ALLOGRAFT TERTIARY LYMPHOID ORGAN DEVELOPMENT REQUIRES HUMORAL IMMUNITY." Transplantation Journal 90 (July 2010): 485. http://dx.doi.org/10.1097/00007890-201007272-00899.

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20

Segerer, S., and D. Schlöndorff. "B cells and tertiary lymphoid organs in renal inflammation." Kidney International 73, no. 5 (March 2008): 533–37. http://dx.doi.org/10.1038/sj.ki.5002734.

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21

Nayar, S., J. Campos, T. Cloake, S. Bowman, M. Bombardieri, C. Pitzalis, S. Luther, C. Buckley, and F. Barone. "SAT0005 IL22 Regulates Autoantibody Production by Inducing Lymphoid Chemokine Expression in Tertiary Lymphoid Organs." Annals of the Rheumatic Diseases 74, Suppl 2 (June 2015): 651.2–651. http://dx.doi.org/10.1136/annrheumdis-2015-eular.5049.

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22

Xu, Xiaoguang, Yong Han, Qiang Wang, Ming Cai, Yeyong Qian, Xinying Wang, Haiyan Huang, Liang Xu, Li Xiao, and Bingyi Shi. "Characterisation of Tertiary Lymphoid Organs in Explanted Rejected Donor Kidneys." Immunological Investigations 45, no. 1 (December 28, 2015): 38–51. http://dx.doi.org/10.3109/08820139.2015.1085394.

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23

Ciccia, F., A. Rizzo, R. Alessandro, G. Guggino, S. Croci, S. Raimondo, A. Cavazza, C. Salvarani, and G. Triolo. "SAT0023 Artery Tertiary Lymphoid Organs Occur in Giant Cell Arteritis." Annals of the Rheumatic Diseases 75, Suppl 2 (June 2016): 672.1–672. http://dx.doi.org/10.1136/annrheumdis-2016-eular.1383.

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24

Berteloot, Laureline, Thierry Jo Molina, Julie Bruneau, Capucine Picard, Vincent Barlogis, Véronique Secq, Chrystelle Abdo, et al. "Alternative pathways for the development of lymphoid structures in humans." Proceedings of the National Academy of Sciences 118, no. 29 (July 14, 2021): e2108082118. http://dx.doi.org/10.1073/pnas.2108082118.

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Lymphoid tissue inducer (LTi) cells are critical for inducing the differentiation of most secondary lymphoid organs (SLOs) in mice. In humans, JAK3 and γc deficiencies result in severe combined immunodeficiency (SCIDs) characterized by an absence of T cells, natural killer cells, innate lymphoid cells (ILCs), and presumably LTi cells. Some of these patients have undergone allogeneic stem cell transplantation (HSCT) in the absence of myeloablation, which leads to donor T cell engraftment, while other leukocyte subsets are of host origin. By using MRI to look for SLOs in nine of these patients 16 to 44 y after HSCT, we discovered that SLOs were exclusively found in the three areas of the abdomen that drain the intestinal tract. A postmortem examination of a child with γc-SCID who had died 3.5 mo after HSCT showed corticomedullary differentiation in the thymus, T cell zones in the spleen, and the appendix, but in neither lymph nodes nor Peyer patches. Tertiary lymphoid organs were observed in the lung. No RAR-related orphan receptor-positive LTi cells could be detected in the existing lymphoid structures. These results suggest that while LTi cells are required for the genesis of most SLOs in humans, SLO in the appendix and in gut-draining areas, as well as tertiary lymphoid organs, can be generated likely by LTi cell-independent mechanisms.

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Pillai, Shiv, and Faisal Alsufyani. "Winning with the B team?" Science Immunology 5, no. 44 (February 7, 2020): eabb0236. http://dx.doi.org/10.1126/sciimmunol.abb0236.

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26

Rustamkhanov, R. A., K. Sh Gantsev, and D. S. Tursumetov. "Tertiary Lymphoid Structures and Cancer Prognosis (Brief Review)." Creative surgery and oncology 9, no. 4 (January 24, 2020): 293–96. http://dx.doi.org/10.24060/2076-3093-2019-9-4-293-296.

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This brief review is devoted to the role of tertiary lymphoid structures in oncological processes. A number of research studies carried out over the past ten years have shed light on the functions of such structures in various diseases, as well as their role in the progression of the pathological process or resolution of a disease. The data presented in some research works confirms the relationship between the presence of tumour-specific (tumour-associated) tertiary lymphoid structures and a favourable prognosis in patients with various oncological diseases, which suggests the participation of tertiary lymphoid structures in effective local antitumour immune responses. However, no reliable evidence has so far been obtained that could confirm the contribution of tertiary lymphoid structures to immune processes in vivo, with the available information being largely of a correlative character. It should be emphasized that the clinical significance of tertiary lymphoid structures ranges from a destructive to protective impact, which indicates the need for an improved understanding of the structure and case-specific function of these organs before conducting clinical targeting.

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Buckley, Christopher D., Francesca Barone, Saba Nayar, Cecile Bénézech, and Jorge Caamaño. "Stromal Cells in Chronic Inflammation and Tertiary Lymphoid Organ Formation." Annual Review of Immunology 33, no. 1 (March 21, 2015): 715–45. http://dx.doi.org/10.1146/annurev-immunol-032713-120252.

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28

Magrone, Thea, and Emilio Jirillo. "Development and Organization of the Secondary and Tertiary Lymphoid Organs: Influence of Microbial and Food Antigens." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 2 (February 7, 2019): 128–35. http://dx.doi.org/10.2174/1871530319666181128160411.

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Background:Secondary lymphoid organs (SLO) are distributed in many districts of the body and, especially, lymph nodes, spleen and gut-associated lymphoid tissue are the main cellular sites. On the other hand, tertiary lymphoid organs (TLO) are formed in response to inflammatory, infectious, autoimmune and neoplastic events. </P><P> Developmental Studies: In the present review, emphasis will be placed on the developmental differences of SLO and TLO between small intestine and colon and on the role played by various chemokines and cell receptors. Undoubtedly, microbiota is indispensable for the formation of SLO and its absence leads to their poor formation, thus indicating its strict interaction with immune and non immune host cells. Furthermore, food antigens (for example, tryptophan derivatives, flavonoids and byphenils) bind the aryl hydrocarbon receptor on innate lymphoid cells (ILCs), thus promoting the development of postnatal lymphoid tissues. Also retinoic acid, a metabolite of vitamin A, contributes to SLO development during embryogenesis. Vitamin A deficiency seems to account for reduction of ILCs and scarce formation of solitary lymphoid tissue. </P><P> Translational Studies: The role of lymphoid organs with special reference to intestinal TLO in the course of experimental and human disease will also be discussed. </P><P> Future Perspectives: Finally, a new methodology, the so-called “gut-in-a dish”, which has facilitated the in vitro interaction study between microbe and intestinal immune cells, will be described.

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29

Jeevanandam, Advait, Kelli Connolly, and Nikhil Joshi. "Abstract B032: Spatial study of tertiary lymphoid structures in lung adenocarcinoma using 3D lightsheet whole-organ Imaging and machine learning-based quantification." Cancer Research 84, no. 22_Supplement (November 17, 2024): B032. http://dx.doi.org/10.1158/1538-7445.tumbody-b032.

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Abstract Lung Adenocarcinoma (LUAD) leads in cancer deaths worldwide. Immune Checkpoint blockade (ICB) therapy has improved patient survival of some subtypes (like Kras oncogene-driven; loss of tumor-suppressor p53– “KP”), but not others (Kras oncogene-driven; loss of LKB1– “KL”). Some studies suggest the poorly inflamed KL tumor environment reduces T cell infiltration. However, the impact of other immune mechanisms/cell types on overall ICB-responsiveness remains understudied. Tertiary lymphoid structures (TLSs) are T/B cell aggregates organized by various cell types that form within inflamed non-lymphoid organs. Recent studies have strongly correlated tumor-associated TLSs (TA-TLSs) with positive clinical outcomes and are predictive of patient responders to immunotherapy in many solid tumor types. Thus, understanding the mechanistic factors that sustain mature TA-TLSs will provide more clarity on what molecularly entails an optimal immune response within an ICB-treated patient. To that end, a major advancement has been our knowledge of TA-TLS phenotypic markers driven through developments in multiplex immunofluorescence imaging of 2D tissue sections. However, tissue sectioning destroys the organ architecture, providing limited spatial information over a small field of view. Therefore, non-destructive 3D fluorescent imaging of whole organs, and lightsheet fluorescence microscopy (LSFM) can provide a novel and broader global view of multicellular structures, like TA-TLSs within the whole organ. By using the Blaze ultramicroscope, we imaged whole lung lobes from our novel autochthonous neoantigen-induced lung adenocarcinoma cancer models of KP and KL mice based on our previously published immunogenic KP x NINJA (inversion-induced joined neoantigen) model, which relies on Cre- recombinase activity dependent activation of KrasLox-Stop-Lox (LSL)G12D and deletion of p53fl/fl. Then, doxycycline and tamoxifen administration lead to lung-specific promoter [club cell secretory protein (CCSP)-rtTA] dependent expression of NINJA. We have also developed novel image segmentation methods using machine learning tools in Imaris 10.2 to identify tumors and immune cell clusters, enabling the quantification of the distance and volume of observable tumors and TLSs in the entire organ, which to our knowledge has not been previously attempted. Using this novel imaging and quantification pipeline, we recently discovered that while KP-NINJA lungs produce many TA-TLSs, the KL tumors (compared to KP) lack organized TA-TLSs, and that intriguingly, B-cells are sparsely sequestered near the main bronchus, away from tumors, resembling small bronchi-associated lymphoid structures (BALTs) that typically form in inflamed lungs. We are concurrently doing 2D multiplex cyclic-immunofluorescence imaging to characterize the variety of other cell types present in TLSs of KP-NINJA vs KL-NINJA and more closely understand the molecular cues sustaining TA-TLSs, providing clarity on what entails an “optimal” immune response within an ICB-treated patient. Citation Format: Advait Jeevanandam, Kelli Connolly, Nikhil Joshi. Spatial study of tertiary lymphoid structures in lung adenocarcinoma using 3D lightsheet whole-organ Imaging and machine learning-based quantification [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Tumor-body Interactions: The Roles of Micro- and Macroenvironment in Cancer; 2024 Nov 17-20; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2024;84(22_Suppl):Abstract nr B032.

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Adoke, Kasimu, and Sanusi Haruna. "10 Tertiary lymphoid structure in pancreatic ductal adenocarcinoma; a potential target in an immunologically inert malignancy." Journal for ImmunoTherapy of Cancer 9, Suppl 2 (November 2021): A10. http://dx.doi.org/10.1136/jitc-2021-sitc2021.010.

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BackgroundTertiary lymphoid structure (TLS) are immune aggregates with various degrees of organization that forms outside of secondary lymphoid organ in response to chronic inflammation, infection or tumours.1 2 TLS like secondary lymphoid organ, has defined T cell zones, B cell zones, high endothelial venules (HEV) and matured dendritic cells. They have been shown to correlate with increase patient survival in many tumours. Pancreatic ductal carcinoma (PDAC) is generally believed to be immunologically inert, low tumour mutation burden (TMB) and poor response to checkpoint blockade. Recent findings in some patients with PDAC shows significant intratumoral cytotoxic T cell infiltration and a high Inflammatory signature. Since current immunotherapy aim to enhance CD 8+ T cells, we aim to investigate the contribution of humoral immunity in patients with TLS in PDAC.MethodsTissue blocks were obtained from departmental archive and sections were cut and stained with routine H&E of all patients who underwent surgery for pancreatic cancer from 2015–2021 at Federal Medical Centre Birnin Kebbi. Serial sections were done at 5µ and four immunohistochemical stains CD 3, CD8, CD20 and PD-L1 were used. Statistical analysis was done using spss version 24.ResultsA total of nine cases of PDAC were diagnosed during the period with a Male Female ratio of 1:1.25 with an age range of 40–68 years and a mean age of 57.7±8.4. Five cases (55.6%) of PDAC showed TLS with marked expression of CD20 B+ cells seen in all five cases (figures 1 and 2). Also expressed are CD 8+ cytotoxic T cells and PD-L1. Prognosis was better in patients with TLS compare with those without TLS.Abstract 10 Figure 1TLS in pancreatic ductal adenocarcinoma.Abstract 10 Figure 2CD 20 stain in TLSConclusionsTLS can be a potential therapeutic target to explore in the future for treatment of some cancers including PDAC through induction of TLS formation in inert tumours or B lymphocyte specific target.ReferencesPitzalis C, Jones GW, Bombardieri M, Jones S. Ectopic lymphoid like structures in infection, cancer and autoimmunity. Nat Rev Immunol 2014; 14: 447–462.Neyt K, Perros F, Geurtsvan C, Hammad H. Lambrecht B. Tertiary lymphoid organs in infection and autoimmunity. Trends Immunol 2012; 33: 297–305.Ethics ApprovalEthical Approval was obtained for this study with Ethics number KSHREC Registration Number:104:6/2019ConsentN/A

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Deng, Shuzhe, Xinxin Yang, Lin He, Yunjing Hou, and Hongxue Meng. "Tertiary Lymphoid Structures in Microorganism-Related Cancer." Cancers 16, no. 20 (October 12, 2024): 3464. http://dx.doi.org/10.3390/cancers16203464.

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Tertiary lymphoid structures (TLSs) are ectopic lymphoid tissues formed by the accumulation of lymphocytes and other components outside lymphoid organs. They have been shown to be widespread in cancers and have predictive effects on prognosis and immunotherapy efficacy; however, there is no standardized measurement guide. This paper provides a reference for future research. Moreover, the induction strategy for the formation mechanism of TLSs is a new direction for future cancer treatment, such as cancer vaccines for microorganisms. The effects of microorganisms on cancer are dual. The role of microorganisms, including bacteria, parasites, viruses, and fungi, in promoting cancer has been widely confirmed. However, the specific mechanism of their tumor suppressor effect, particularly the promotion of TLS formation, is currently unknown. In this review, we summarize the role of TLSs in cancer related to microbial infection and provide new ideas for further understanding their mechanisms of action in cancer.

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Thaunat, Olivier, Natacha Patey, Chantal Gautreau, Sophie Lechaton, Véronique Fremeaux-Bacchi, Marie-Caroline Dieu-Nosjean, Elisabeth Cassuto-Viguier, et al. "B Cell Survival in Intragraft Tertiary Lymphoid Organs After Rituximab Therapy." Transplantation 85, no. 11 (June 2008): 1648–53. http://dx.doi.org/10.1097/tp.0b013e3181735723.

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Paramasivan, Sathish, Susan Lester, Aden Lau, Judy Ou, Alkis James Psaltis, Peter-John Wormald, and Sarah Vreugde. "Tertiary lymphoid organs: A novel target in patients with chronic rhinosinusitis." Journal of Allergy and Clinical Immunology 142, no. 5 (November 2018): 1673–76. http://dx.doi.org/10.1016/j.jaci.2018.07.024.

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Nasr, Isam W., Qi Li, and Fadi G. Lakkis. "Inhibition of tertiary lymphoid organs in a murine chronic rejection model." Journal of the American College of Surgeons 209, no. 3 (September 2009): S57—S58. http://dx.doi.org/10.1016/j.jamcollsurg.2009.06.137.

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Schaadt, Nadine S., Ralf Schönmeyer, Germain Forestier, Nicolas Brieu, Peter Braubach, Katharina Nekolla, Michael Meyer-Hermann, and Friedrich Feuerhake. "Graph-based description of tertiary lymphoid organs at single-cell level." PLOS Computational Biology 16, no. 2 (February 21, 2020): e1007385. http://dx.doi.org/10.1371/journal.pcbi.1007385.

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Thelen, M., MA García-Márquez, T. Nestler, S. Wagener-Ryczek, J. Lehmann, E. Staib, F. Popp, et al. "P03.03 Organization, function and gene expression of tertiary lymphoid structures in PDAC resembles lymphoid follicles in secondary lymphoid organs." Journal for ImmunoTherapy of Cancer 8, Suppl 2 (October 2020): A23.1—A23. http://dx.doi.org/10.1136/jitc-2020-itoc7.43.

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BackgroundSecondary lymphoid organs (SLO) are involved in induction and enhancement of anti-tumor immune responses on different tumor entities. Recent evidence suggests that anti-tumor immune responses may also be induced or enhanced in the tumor microenvironment in so called tertiary lymphoid structures (TLS). It is assumed that TLS represent a hotspot for T cell priming, B cell activation, and differentiation, leading to cellular and humoral anti-tumor immune response.MethodsFFPE-slides of 120 primary pancreatic ductal adenocarcinoma (PDAC) patients were immunohistochemically (IHC) stained for CD20, CD3, CD8 and HLA-ABC to analyze spatial distribution of tumor-infiltrating lymphocytes. 5-color immunofluorescence staining was performed to further investigate structural components of TLS in comparison to lymphoid follicles in SLOs. Microscope-based laser microdissection and Nanostring-base RNA expression analysis were used to compare gene expression in PDAC, TLS, SLOs and normal pancreatic tissue.ResultsTLS were frequently detected in PDAC and were mainly localized along the invasive tumor margin. In less than 10% of the cases TLS were infiltrating the tumors. Interestingly, 20% of the patients had no TLS. Results of TLS will be correlated with clinical parameters, Immunoscore and immune escape mechanisms. 5-color Immunofluorescence staining revealed similar organization and function of TLS and SLO. Finally, gene expression analyzed by Nanostring revealed largely overlapping expression patterns in TLS and SLO.ConclusionsThe results clearly demonstrate close similarities between SLO and TLS in terms of composition, distribution and gene expression Patterns.Disclosure InformationM. Thelen: None. M.A. García-Márquez: None. T. Nestler: None. S. Wagener-Ryczek: None. J. Lehmann: None. E. Staib: None. F. Popp: None. F. Gebauer: None. P. Lohneis: None. M. Odenthal: None. S. Merkelbach-Bruse: None. C. Bruns: None. K. Wennhold: None. M. von Bergwelt-Baildon: None. H.A. Schlößer: None.

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Pei, Guangchang, Rui Zeng, Min Han, Panli Liao, Xuan Zhou, Yueqiang Li, Ying Zhang, et al. "Renal Interstitial Infiltration and Tertiary Lymphoid Organ Neogenesis in IgA Nephropathy." Clinical Journal of the American Society of Nephrology 9, no. 2 (November 21, 2013): 255–64. http://dx.doi.org/10.2215/cjn.01150113.

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Frasca, Daniela, and Bonnie B. Blomberg. "Adipose Tissue: A Tertiary Lymphoid Organ: Does It Change with Age?" Gerontology 66, no. 2 (August 14, 2019): 114–21. http://dx.doi.org/10.1159/000502036.

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Mounzer, Rawad H., Oyvind S. Svendsen, Peter Baluk, Cheryl M. Bergman, Timothy P. Padera, Helge Wiig, Rakesh K. Jain, Donald M. McDonald, and Nancy H. Ruddle. "Lymphotoxin-alpha contributes to lymphangiogenesis." Blood 116, no. 12 (September 23, 2010): 2173–82. http://dx.doi.org/10.1182/blood-2009-12-256065.

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Abstract Lymphotoxin-α (LTα), lymphotoxin-β (LTβ), and tumor necrosis factor-α (TNFα) are inflammatory mediators that play crucial roles in lymphoid organ development. We demonstrate here that LTα also contributes to the function of lymphatic vessels and to lymphangiogenesis during inflammation. LTα−/− mice exhibited reduced lymph flow velocities and increased interstitial fluid pressure. Airways of LTβ−/− mice infected with Mycoplasma pulmonis had significantly more lymphangiogenesis than wild type (WT) or LTα−/− mice, as did the skin draining immunization sites of LTβ−/− mice. Macrophages, B cells, and T cells, known sources of LT and TNFα, were apparent in the skin surrounding the immunization sites as were LTα, LTβ, and TNFα mRNAs. Ectopic expression of LTα led to the development of LYVE-1 and Prox1-positive lymphatic vessels within tertiary lymphoid organs (TLOs). Quantification of pancreatic lymphatic vessel density in RIPLTαLTβ−/− and WT mice revealed that LTα was sufficient for inducing lymphangiogenesis and that LTβ was not required for this process. Kidneys of inducible LTα transgenic mice developed lymphatic vessels before the appearance of obvious TLOs. These data indicate that LTα plays a significant role in lymphatic vessel function and in inflammation-associated lymphangiogenesis.

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Lu, Theresa T., Hajeong Kim, and Xiaojing Ma. "IL-17, a new kid on the block of tertiary lymphoid organs." Cellular & Molecular Immunology 9, no. 1 (September 19, 2011): 3–4. http://dx.doi.org/10.1038/cmi.2011.34.

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Huang, Hsin-Ying, and Sanjiv A. Luther. "Expression and function of interleukin-7 in secondary and tertiary lymphoid organs." Seminars in Immunology 24, no. 3 (June 2012): 175–89. http://dx.doi.org/10.1016/j.smim.2012.02.008.

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Wirsing, A., O. Rikardsen, S. E. Steigen, L. Uhlin-Hansen, and E. Hadler-Olsen. "886: Prognostic relevance of tertiary lymphoid organs in oral squamous cell carcinoma." European Journal of Cancer 50 (July 2014): S216. http://dx.doi.org/10.1016/s0959-8049(14)50786-1.

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Zhai, Yunhao, Pranav Prabhala, Lucas Barck, Min Wen Ku, Aditya Patil, Viktor Horvath, Russell A. Gould, Donald E. Ingber, and Girija Goyal. "Abstract B063: Tertiary lymphoid organogenesis and lymphocyte activation in human organ chips." Cancer Research 84, no. 2_Supplement (January 16, 2024): B063. http://dx.doi.org/10.1158/1538-7445.panca2023-b063.

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Abstract The rates of tertiary lymphoid organ (TLO) formation in pancreatic cancer are very low but patients with TLO have dramatically better survival rates. Our goal is to understand how pancreatic cancer suppresses TLO so that we can improve patient survival and reduce recurrence. We integrated human cell lines from pancreatic and lung cancer with either high or low PDL1/L2 expression into our previously described lymphoid follicle (LF) chip (Goyal et al., Adv. Sci, 2022), where peripheral blood mononuclear cells are induced to form 3D TLO-like structures. The hot lung cancer cell line, which expressed high levels of PDL1/L2 and a “hot” phenotype in published murine studies, produced a high levels of cytokines and stimulated increased TLO formation in the LF chip. In contrast, the cold lung and pancreatic cell lines did not induce the cytokine signature or TLOs. Importantly, TLO formation correlated with increased B cell activation, anti-tumor CD8 activity and tumor cell death. We have coupled this in vitro study with analysis of the pancreatic cancer transcriptome from the Cancer Genome Atlas to identify therapeutic targets to promote TLO formation in pancreatic cancer. In ongoing studies, we are assessing the functionality of the lung cancer TLO in vitro and in vivo and identifying therapeutics that may improve TLO formation in pancreatic cancer. Citation Format: Yunhao Zhai, Pranav Prabhala, Lucas Barck, Min Wen Ku, Aditya Patil, Viktor Horvath, Russell A. Gould, Donald E. Ingber, Girija Goyal. Tertiary lymphoid organogenesis and lymphocyte activation in human organ chips [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Pancreatic Cancer; 2023 Sep 27-30; Boston, Massachusetts. Philadelphia (PA): AACR; Cancer Res 2024;84(2 Suppl):Abstract nr B063.

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Galy, A., M. Clément, P. Bruneval, F. Hyafil, T. Papo, A. Nicoletti, and K. Sacré. "Organes lymphoïdes tertiaires dans l’artérite de Takayasu : les lymphocytes B sont-ils impliqués dans la pathogénie ?" La Revue de Médecine Interne 37 (June 2016): A106. http://dx.doi.org/10.1016/j.revmed.2016.04.046.

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Weiss, J. M., P. Cufi, R. Le Panse, and S. Berrih-Aknin. "The thymus in autoimmune Myasthenia Gravis: Paradigm for a tertiary lymphoid organ." Revue Neurologique 169, no. 8-9 (August 2013): 640–49. http://dx.doi.org/10.1016/j.neurol.2013.02.005.

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Reed, Hasina Outtz, Liqing Wang, Jarrod Sonett, Mei Chen, Jisheng Yang, Larry Li, Petra Aradi, et al. "Lymphatic impairment leads to pulmonary tertiary lymphoid organ formation and alveolar damage." Journal of Clinical Investigation 129, no. 6 (May 20, 2019): 2514–26. http://dx.doi.org/10.1172/jci125044.

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Műzes, Györgyi, Bettina Bohusné Barta, and Ferenc Sipos. "Colitis and Colorectal Carcinogenesis: The Focus on Isolated Lymphoid Follicles." Biomedicines 10, no. 2 (January 21, 2022): 226. http://dx.doi.org/10.3390/biomedicines10020226.

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Gut-associated lymphoid tissue is one of the most diverse and complex immune compartments in the human body. The subepithelial compartment of the gut consists of immune cells of innate and adaptive immunity, non-hematopoietic mesenchymal cells, and stem cells of different origins, and is organized into secondary (and even tertiary) lymphoid organs, such as Peyer’s patches, cryptopatches, and isolated lymphoid follicles. The function of isolated lymphoid follicles is multifaceted; they play a role in the development and regeneration of the large intestine and the maintenance of (immune) homeostasis. Isolated lymphoid follicles are also extensively associated with the epithelium and its conventional and non-conventional immune cells; hence, they can also function as a starting point or maintainer of pathological processes such as inflammatory bowel diseases or colorectal carcinogenesis. These relationships can significantly affect both physiological and pathological processes of the intestines. We aim to provide an overview of the latest knowledge of isolated lymphoid follicles in colonic inflammation and colorectal carcinogenesis. Further studies of these lymphoid organs will likely lead to an extended understanding of how immune responses are initiated and controlled within the large intestine, along with the possibility of creating novel mucosal vaccinations and ways to treat inflammatory bowel disease or colorectal cancer.

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Sunyer, J. Oriol, Yasuhiro Shibasali, Fumio Takizawa, Ding Yang, Pierre Boudinot, and Aleksei Krasnov. "IDENTIFICATION OF PRIMORDIAL ORGANIZED LYMPHOID STRUCTURE IN THE SPLEEN OF TELEOST FISH." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 92.40. http://dx.doi.org/10.4049/jimmunol.204.supp.92.40.

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Abstract Induction of adaptive immune responses in higher vertebrate species occur within organized lymphoid structures (e.g. lymph nodes, Peyer’s patches). It has been proposed that such structures emerged throughout evolutionary time with the goal to maximize encounters between antigens, antigens-presenting cells and B-T lymphocytes. Fish lack such structures and thus, it remains unknown how and where antigen-specific immunoglobulin responses are induced in these species. To understand how systemic immune responses are induced in teleost lymphoid organs, Rainbow Trout were immunized with several soluble protein antigens. Overall, our results identified the spleen as the major site for CD4+ T and IgM+ B cell proliferation in systemic lymphoid organs upon immunization. The proliferating splenic IgM+ B cells were frequently observed as clusters in the vicinity of melano-macrophage centers. Moreover, in these areas we observed aggregates of B and T lymphocytes with a loose organized structure reminiscent of the cellular architecture frequently associated with tertiary lymphoid organs. Laser dissection microdissection of these areas enabled us to evaluating the immunoglobulin IgM repertoires within these structures upon immunization. Critically, repertoire analysis identified processes of antigen-specific B cell clonal expansion. In conclusion, these data points to the previously unrecognized existence of primordial semi-organized lymphoid tissue in the spleen of teleost fish in which adaptive IgM immune responses are induced. Our findings provide strong evidence that the induction of antigen-specific immune responses in all bony vertebrates requires the formation of organized or semi-organized lymphoid structures.

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Willard-Mack, Cynthia L., Susan A. Elmore, William C. Hall, Johannes Harleman, C. Frieke Kuper, Patricia Losco, Jerold E. Rehg, et al. "Nonproliferative and Proliferative Lesions of the Rat and Mouse Hematolymphoid System." Toxicologic Pathology 47, no. 6 (August 2019): 665–783. http://dx.doi.org/10.1177/0192623319867053.

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The INHAND Project (International Harmonization of Nomenclature and Diagnostic Criteria for Lesions in Rats and Mice) is a joint initiative of the Societies of Toxicologic Pathology from Europe (ESTP), Great Britain (BSTP), Japan (JSTP), and North America (STP) to develop an internationally accepted nomenclature for proliferative and nonproliferative changes in rats and mice. The purpose of this publication is to provide a standardized nomenclature for classifying changes observed in the hematolymphoid organs, including the bone marrow, thymus, spleen, lymph nodes, mucosa-associated lymphoid tissues, and other lymphoid tissues (serosa-associated lymphoid clusters and tertiary lymphoid structures) with color photomicrographs illustrating examples of the lesions. Sources of material included histopathology databases from government, academia, and industrial laboratories throughout the world. Content includes spontaneous lesions as well as lesions induced by exposure to test materials. The nomenclature for these organs is divided into 3 terminologies: descriptive, conventional, and enhanced. Three terms are listed for each diagnosis. The rationale for this approach and guidance for its application to toxicologic pathology are described in detail below.

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Huppé, Carole-Ann, Pascale Blais Lecours, Ariane Lechasseur, Mathieu C. Morissette, and David Marsolais. "S1P1 regulation of pulmonary tertiary lymphoid tissues." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 53.16. http://dx.doi.org/10.4049/jimmunol.198.supp.53.16.

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Abstract Pulmonary tertiary lymphoid tissues (TLT) emerge as central regulators of antigen-specific responses in the lung and they have been associated with the severity of chronic respiratory diseases such as hypersensitivity pneumonitis (HP). The sphingosine-1-phosphate receptor S1P1 is a potent modulator of lymphoid organ biology and of the TH17 response, which is often associated with HP and TLT formation in the lung. We recently identified a novel immunogenic agent commonly found in the bioaerosols of working environments that induces an HP-like disease and potently stimulates TLT formation in the lung. We first aimed to determine if the ability of this agent to induce TLTs was related to their propensity to trigger a TH17 response in the lung. Secondly, we determined whether or not S1P1 acts as a modulator of pulmonary TLTs. Mice were exposed intra-nasally to Methanosphaera stadtmanae (MSS) for a 3-weeks time period in order to induce TLT formation. Upon MSS rechallenge, Il-17 expression was increased by 3 fold in the lung supporting the involvement of this cytokine in the current model. Among five homeostatic chemokines/proinflammatory cytokines tested, we found that CXCL13 was the most significantly increased by the MSS rechallenge (4.9-fold), supporting its involvement in TLT formation in response to MSS. S1P1 pharmacological agonism led to a 50% inhibition of Il-17 and Cxcl13 expression in the lung, which translated into a full inhibition of TLT expansion in response to the MSS rechallenge; and into a 77% alleviation of the pulmonary neutrophilic response. This study unravels a role for the S1P pathway in the regulation of TLTs as well as its interplay with the TH17 response in the lung.

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