Ī 2011 report of frequent somatic mutations in the tet methylcytosine dioxygenase 2 ( TET2) gene provided insight into AITL genetics, as did discovery soon after of recurrent somatic mutations in DNA methyltransferase 3A ( DNMT3A) and isocitrate dehydrogenase 2 ( IDH2). It is noteworthy that Tfh cell physiology was defined and characterized in parallel. These findings confirmed the idea that Tfh cells are the normal cellular counterparts of AITL tumor cells. Global gene expression patterns seen in whole AITL tissues and isolated tumor cells were then shown to resemble those seen in Tfh cells. By the early 2000s, important insight had been gained by the discovery of expression of CD10 and C-X-C motif chemokine ligand 13 (CXCL13) in clear cells. In the 1990s a consensus was gradually reached that “clear cells” rather than “immunoblasts” represented neoplastic cells. Such confusion was in part attributable to uncertainty over tumor cell identity. WHO classifications followed this designation, although debate continued until the 2000s over whether true nonneoplastic AILD/IBL exists and whether it represents a premalignant state. In 1994 the term “angioimmunoblastic T-cell lymphoma” was introduced in the Revised European and American Classification of Lymphoid Neoplasms. At the same time, accurate diagnosis of AILD/IBL was facilitated by staining of follicular dendritic cells (FDCs) with anti-CD21 and -CD23 antibodies. By the late 1980s, the consensus was that most cases described as AILD/IBL were T-cell lymphoma. Later, a proportion of AILD/IBL cases were diagnosed as malignant lymphoma of either B-cell or T-cell origin. Early on, however, investigators recognized that the condition was marked by a broad histologic spectrum and speculated that some patients’ disease might be neoplastic, although they could not make the distinction. All groups initially proposed that the disease was a nonneoplastic, hyperimmune reaction. In the early-mid 1970’s, different groups proposed what turned out to be a fundamentally identical disease based on observations of independent patient cohorts, namely, a condition variously described as immunodysblastic disease, angioimmunoblastic lymphadenopathy with dysproteinemia (AILD), or immunoblastic lymphadenopathy (IBL).
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