Cutting Edge: Ectopic Expression of the Chemokine TCA4/SLC Is Sufficient to Trigger Lymphoid Neogenesis

Fan, Lian; Reilly, Christina R.; Luo, Yi; Dorf, Martin E.; Lo, David

doi:10.4049/jimmunol.164.8.3955

Cited by 174 publications

(145 citation statements)

References 30 publications

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“…31 Furthermore, it has been demonstrated that CCL21 could participate itself in lymphoid tissue development and organization in a transgenic model where the CCL21 gene was expressed in pancreatic islets. 32 In addition, CCL21 has been demonstrated to induce an angiostatic activity through interaction with another receptor CXCR3. 21,23 These dual properties are profitable to induce a strong antitumor response.…”

Section: Discussionmentioning

confidence: 99%

Synergistic antitumor effect by coexpression of chemokine CCL21/SLC and costimulatory molecule LIGHT

et al. 2004

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To establish a more efficient treatment for immunotherapy against solid tumors, we have evaluated the antitumor effect by coexpression of a chemokine CCL21/secondary lymphoid tissue chemokine and a costimulatory molecule LIGHT in colon carcinoma C26. C26 cells expressing either CCL21 or LIGHT exhibited a significantly reduced tumor growth in vivo, and mice inoculated with these cells showed a prolonged survival, but eventually all these mice died. In contrast, C26 cells expressing both CCL21 and LIGHT exhibited a minimal tumor growth in vivo, and all these mice survived healthily with a tumor remission and consequently acquired a strong protective immunity. A markedly increased infiltration of mature dendritic cells (DCs), and CD8 þ T cells was observed in the tumor mass, and their spleen cells showed a greatly enhanced cytotoxic T lymphocyte (CTL) activity against C26 tumor and interferon (IFN)-g production. Neutralization of IFN-g or depletion of CD8 þ or CD4 þ T cells significantly reduced the antitumor activity. These results suggest that the combined treatment with CCL21 and LIGHT is able to induce a synergistic antitumor effect to eradicate tumor completely by greatly enhancing tumor-infiltration of lymphocytes including mature DCs and CD8 þ T cells, resulting in markedly augmented CTL activity and IFN-g production.

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Section: Discussionmentioning

confidence: 99%

Synergistic antitumor effect by coexpression of chemokine CCL21/SLC and costimulatory molecule LIGHT

et al. 2004

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“…For example, transgenic expression of Ccl21 in the pancreas promotes ELFs that display T‐cell and B‐cell segregation, HEV and stromal reticulum. However, this response is context dependent and Ccl21 in the skin fails to initiate lymphoneogenesis 54, 55. Histological features of ELFs are seen in various chronic inflammatory diseases and are clinically observed in the lung, joint synovium, liver, thymus, and salivary and thyroid glands (for a comprehensive review of ELFs in human disease refer to Pitzalis et al 10…”

Section: Homeostatic Chemokines In Elf Developmentmentioning

confidence: 99%

Ectopic lymphoid follicles: inducible centres for generating antigen‐specific immune responses within tissues

2015

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SummaryLymphoid neogenesis is traditionally viewed as a pre‐programmed process that promotes the formation of lymphoid organs during development. Here, the spatial organization of T and B cells in lymph nodes and spleen into discrete structures regulates antigen‐specific responses and adaptive immunity following immune challenge. However, lymphoid neogenesis is also triggered by chronic or persistent inflammation. Here, ectopic (or tertiary) lymphoid organs frequently develop in inflamed tissues as a response to infection, auto‐immunity, transplantation, cancer or environmental irritants. Although these structures affect local immune responses, the contribution of these lymphoid aggregates to the underlining pathology are highly context dependent and can elicit either protective or deleterious outcomes. Here we review the cellular and molecular mechanisms responsible for ectopic lymphoid neogenesis and consider the relevance of these structures in human disease.

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“…Just as with LNs, TLO formation can be induced through overexpression of CCL21, CCL19 and CXCL13 in a tissuespecific manner [65,99,100]. Furthermore, they may accumulate antigen and APCs, bypassing the LN and therefore restricting normal LN function [62,101].…”

Section: Tertiary Lymphoid Organsmentioning

confidence: 99%

Role of Lymphatic Vessels in Tumor Immunity: Passive Conduits or Active Participants?

Lund

Swartz

2010

J Mammary Gland Biol Neoplasia

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Research in lymphatic biology and cancer immunology may soon intersect as emerging evidence implicates the lymphatics in the progression of chronic inflammation and autoimmunity as well as in tumor metastasis and immune escape. Like the blood vasculature, the lymphatic system comprises a highly dynamic conduit system that regulates fluid homeostasis, antigen transport and immune cell trafficking, which all play important roles in the progression and resolution of inflammation, autoimmune diseases, and cancer. This review presents emerging evidence that lymphatic vessels are active modulators of immunity, perhaps fine-tuning the response to adjust the balance between peripheral tolerance and immunity. This suggests that the tumor-associated lymphatic vessels and draining lymph node may be important in tumor immunity which in turn governs metastasis.

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Cutting Edge: Ectopic Expression of the Chemokine TCA4/SLC Is Sufficient to Trigger Lymphoid Neogenesis

Cited by 174 publications

References 30 publications

Synergistic antitumor effect by coexpression of chemokine CCL21/SLC and costimulatory molecule LIGHT

Synergistic antitumor effect by coexpression of chemokine CCL21/SLC and costimulatory molecule LIGHT

Ectopic lymphoid follicles: inducible centres for generating antigen‐specific immune responses within tissues

Role of Lymphatic Vessels in Tumor Immunity: Passive Conduits or Active Participants?

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