LipoxinA 4modulates adaptive immunity by decreasing memoryB ‐cell responses via anALX /FPR 2‐dependent mechanism
Autor: | Sesquile Ramon, Charles N. Serhan, Richard P. Phipps, Simona Bancos |
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Rok vydání: | 2013 |
Předmět: |
Lipoxin
Innate immune system biology Monocyte Immunology Inflammation Acquired immune system Immunoglobulin G chemistry.chemical_compound Immune system medicine.anatomical_structure chemistry biology.protein medicine Immunology and Allergy lipids (amino acids peptides and proteins) medicine.symptom Memory B cell |
Zdroj: | European Journal of Immunology. 44:357-369 |
ISSN: | 1521-4141 0014-2980 |
Popis: | Specialized proresolving mediators are endogenous bioactive lipid molecules that play a fundamental role in the regulation of inflammation and its resolution. Lipoxins and other specialized proresolving mediators have been identified in important immunological tissues including bone marrow, spleen, and blood. Lipoxins regulate functions of the innate immune system including the promotion of monocyte recruitment and increase macrophage phagocytosis of apoptotic neutrophils. A major knowledge gap is whether lipoxins influence adaptive immune cells. Here, we analyzed the actions of lipoxin A4 (LXA4) and its receptor ALX/FPR2 on human and mouse B cells. LXA4 decreased IgM and IgG production on activated human B cells through ALX/FPR2-dependent signaling, which downregulated NF-κB p65 nuclear translocation. LXA4 also inhibited human memory B-cell antibody production and proliferation, but not naive B-cell function. Lastly, LXA4 decreased antigen-specific antibody production in an OVA immunization mouse model. To our knowledge, this is the first description of the actions of lipoxins on human B cells, demonstrating a link between resolution signals and adaptive immunity. Regulating antibody production is crucial to prevent unwanted inflammation. Harnessing the ability of lipoxins to decrease memory B-cell antibody production can be beneficial to threat inflammatory and autoimmune disorders. |
Databáze: | OpenAIRE |
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