Anti-CD7 (extracellular domain) polyclonal antibody

Adult T-cell leukemia/lymphoma (ATL), a human T-lymphotropic virus type 1 (HTLV-1)-associated disease, has a highly variable clinical course and four subtypes with therapeutic and prognostic implications. However, there are overlapping features between ATL subtypes and between ATL and nonmalignant (non-ATL) HTLV-1 infection complicating diagnosis and prognostication. To further refine the diagnosis and prognosis of ATL, we characterized the immunophenotype of HTLV-1-infected cells in ATL and non-ATL. A retrospective study of peripheral blood samples from 10 HTLV-1-uninfected subjects (UI), 54 HTLV-1-infected patients with non-ATL, and 22 with ATL was performed using flow cytometry. All patients with ATL had CD4(+) CCR4(+) CD26(-) immunophenotype and the frequency of CD4(+) CCR4(+) CD26(-) T cells correlated highly significantly with the proviral load in non-ATL suggesting CD4(+) CCR4(+) CD26(-) as a marker of HTLV-1-infected cells. Further immunophenotyping of CD4(+) CCR4(+) CD26(-) T cells revealed that 95% patients with ATL had a CD7(-) (<= 30% CD7(+) cells), whereas 95% HTLV+ non-ATL had CD7(+) (>30% CD7(+) cells) immunophenotype. All patients with aggressive ATL had a CCR7(+) (>= 30%), whereas 92% with indolent ATL and 100% non-ATL had a CCR7(-) (<30%) immunophenotype. Patients with nonprogressing indolent ATL were CD127(+) but those with progressive lymphocytosis requiring systemic therapy had a CD127(-) (<= 30%) immunophenotype. In summary, HTLV-1-infected cells have a CD4(+) CCR4(+) CD26(-) immunophenotype. Within this population, CD7(-) phenotype suggests a diagnosis of ATL, CCR7(+) phenotype identifies aggressive ATL, while CCR7(-) CD127(-) phenotype identifies progressive indolent ATL.

Morphological and immuno- flow cytometry assisted analysis of peripheral blood and bone marrow are mandatory investigations in the diagnosis of acute leukemia. Cytology and immunophenotyping complement each other primarily because they have as common object malignant cell phenotype as a whole. The aim of our study was to analyze correlations between cytology and immunophenotyping on a group of patients investigated for acute myeloid leukemia. In our study the degree of correlation between blast percentage determined by cytology and immunophenotyping was low (r=0.049). The degree of correlation between myeloperoxidase positivity in cytochemistry and immunophenotyping was also low, with better results for cytochemistry. Expression of immunophenotypic markers was consistent with the composition of our group regarding French-American-British classes, except for HLA-DR (49.0%), TdT (3.77%), CD14 (5.66%), CD15 (5.66%). We also discuss the importance of interpreting with caution positivity for erythroid and megakaryocytic markers and differential diagnosis of cases simultaneously expressing CD7 and CD56. In conclusion, interpretation of immunophenotyping by flow citometry, done in close conjunction with morphology, is mandatory to facilitate the use of optimized sample processing methods and of standardized panels, for both appropriate diagnosis and follow-up.