Abstract
This editorial refers to ‘M1 macrophages act as LTβR-independent lymphoid tissue inducer cells during atherosclerosis-related lymphoid neogenesis’ by K. Guedj et al. , pp. 434–443, this issue. The immune system has evolved to optimize the chances of encounter between rare antigen-specific T and B cells of the adaptive immune system with antigen presenting cells of the innate immune system through development of organized secondary lymphoid organs (SLOs) such as the spleen and lymph nodes. This system efficiently eradicates pathogens, including foreign antigens. However, when antigens are constantly replenished, as in atherosclerosis, this can lead to local or systemic chronic inflammation. Under such conditions, tissues that persistently harbour target antigens are infiltrated by cellular effectors of the immune system, including T cells, B cells, and macrophages as well as dendritic cells and plasma cells. These cellular elements frequently organize themselves anatomically and functionally similar to SLOs, leading to de novo formation of B-cell follicles and T-cell areas by a process called lymphoid neogenesis or tertiary lymphoid organ (TLO) formation. TLOs have been observed in autoimmune diseases such as autoimmune thyroiditis, rheumatoid arthritis, and myasthenia gravis as well as in chronic allograft rejection,1,2 diabetes,3 and in atherosclerosis.4 Whilst the role of TLOs is still yet to be fully elucidated in diseases such as atherosclerosis, there is evidence that like SLOs, they can contribute to immune disease progression.5 For example, B cells in TLOs within lungs of patients with rheumatoid arthritis …
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