Abstract

BackgroundVaccine immune response is impaired in cancer patients. Follicular helper T lymphocytes (cTfh) are essential for high affinity and long lasting humoral response. The objective of this study was to evaluate the role of cTfh in the immune response induced by influenza vaccine in children with acute lymphoblastic leukemia (ALL).MethodsChildren with ALL in maintenance therapy and a control group of healthy children were included. Blood samples were taken on the day of vaccination (D0), and on day 28 (D28). The humoral response was evaluated by haemagglutination inhibition test and frequency of cTfh was studied by flow cytometry.ResultsTwenty-four children with ALL and 8 healthy children were included: 67 and 38% were women, median age of 5 years old in both groups. A 33% (8/24) of patients and 63% (5/8) of controls were seroprotected at D28. Seroprotected children at D28 were significantly older than non-protected ones (10 and 3.6 years respectively, P = 0,004). During follow-up, three children with ALL had influenza infection. An increase of percentage of cTfh cells from D0 to D28 was observed in both groups, but it was significant only in ALL patients (average for ALL, D0-D28: 18–23%, P = 0.003 and average for controls, D0-D28: 22–26%). No differences were found between seroprotected and non-seroprotected children in cTfh cell at D0 or D28. The increase of percentage of cTfh cells from D0 to D28 was observed in both groups, it was significant only in non-seroprotected subjects (average for seroprotected, D0-D28: 21–24% and average for non-seroprotected, D0-D28: 18–24%, P = 0.004).ConclusionChildren with ALL achieved a lower seroprotection than healthy children. After vaccination, both groups had an increase of cTfh cells. We did not found an association between the percentage of cTfh cells and seroprotection at D28. The association between the lack of humoral response and cTfh dysfunction should be evaluated in further studies (We report public funding from Fondecyt grant Nº 11150970).Disclosures All authors: No reported disclosures.

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