expression of CXCL13 and CXCR5 in neoplastic T cells, again pointing to a T FH phenotype. [3][4][5][6][7][8] Coexpression of the CXCR5 chemokine receptor and its ligand CXCL13 suggests an autocrine loop, possibly contributing to the survival of neoplastic T cells. All cases demonstrated coexpression of CD154 in the majority of the neoplastic T cells. This antigen plays a crucial role in GC formation 9 and provides survival signals to follicular B cells. 6 Each case showed significant but variable numbers (10%-100%) of CXCL13 ϩ T cells bearing CD134, whose expression on activated CD4 ϩ T cells either initiates their migration into or causes them to be retained in B follicles. 10 One case coexpressed CD57 in a significant proportion of neoplastic cells, while the remaining cases displayed only a minute fraction of CD57 ϩ CXCL13 ϩ cells that may reflect the residual normal T FH cells. Since proliferating FDCs expressed CXCL13 and are known to express CD40 9 (receptor for CD154) and OX40L 6,10 (ligand for CD134), our data suggest a selective cross-talk between FDCs and neoplastic T cells.Our observations not only fully support the notion of Grogg et al 1 but extend it by a more detailed analysis, establishing that the phenotype of the neoplastic cells (as shown here) is consistent with activated T FH cells localized at the boundary between the mantle zone and the GC light zone. 6 These findings provide direct explanations for some peculiar features of AITL, including B-cell hyperactivation and hypergammaglobulinemia despite gradual reduction of follicular B-cell mass, as well as the follicular outgrowths of FDCs as a result of stimulation by neoplastic T FH cells. Further investigations will be needed to explain loss of follicular B cells, a phenomenon that occurs in advanced cases and may be caused by a disarranged dialogue between neoplastic T FH cells and nonneoplastic B cells. To the editor:Immune thrombocytopenic purpura does not exhibit a disparity in prevalence between African American and white veterans Ethnic, racial, and geographic differences influence virtually all human disease, and certain conditions exhibit well-established differences between Africans and Europeans. 1 Once such differences are identified, it is important to examine them, because etiologic, genetic, and therapeutic heterogeneity may be present. 2,3 In addition, ethnic disparities of all types may be accompanied by For personal use only. on April 29, 2019. by guest www.bloodjournal.org From important social differences influencing medical access or diverse cultural practices with consequences for health care delivery and outcomes. It is therefore crucial to confirm conclusions about putative racial disparities with well-grounded assessments derived from large population-based data to avoid erroneous conclusions.A recent review of previous small studies [4][5][6][7][8][9][10] reported that the proportion of African American patients with immune thrombocytopenic purpura (ITP) was very low compared with the proportion of African American...