AI Article Synopsis
- Angioimmunoblastic T-cell lymphoma (AITL) arises from follicular helper T (Tfh) cells and is difficult to treat due to its resistance to current therapies.
- The progression of AITL involves a complex interaction between neoplastic Tfh cells and B-cells in the tumor microenvironment, similar to processes in germinal centers.
- Recurrent mutations like TET2 and DNMT3A in both Tfh and B-cells hint that their relationship could be a potential target for new treatments, highlighting important signaling mechanisms in AITL's pathobiology.
Article Abstract
Angioimmunoblastic T-cell lymphoma (AITL), the most common form of peripheral T-cell lymphoma, originates from follicular helper T (Tfh) cells and is notably resistant to current treatments. The disease progression and maintenance, at least in early stages, are driven by a complex interplay between neoplastic Tfh and clusters of B-cells within the tumor microenvironment, mirroring the functional crosstalk observed inside germinal centers. This interaction is further complicated by recurrent mutations, such as TET2 and DNMT3A, which are present in both Tfh cells and B-cells. These findings suggest that the symbiotic relationship between these 2 cell types could represent a therapeutic vulnerability. This review examines the key components and signaling mechanisms involved in the synapses between B-cells and Tfh cells, emphasizing their significant role in the pathobiology of AITL and potential as therapeutic targets.
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| http://dx.doi.org/10.1016/j.labinv.2024.102147 | DOI Listing |
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