Anti-Pneumococcal Vaccine-Induced Cellular Immune Responses in Post-Traumatic Splenectomized Individuals
Erişim
info:eu-repo/semantics/closedAccessTarih
2017Yazar
Karasartova, DjursunGazi, Umut
Tosun, Özgür
Güreser, Ayşe Semra
Şahiner, İbrahim Tayfun
Dolapçı, Mete
Taylan Özkan, Hikmet Ayşegül
Üst veri
Tüm öğe kaydını gösterKünye
Karasartova, D., Gazi, U., Tosun, O., Gureser, A. S., Sahiner, I. T., Dolapci, M., & Ozkan, A. T. (2017). Anti-pneumococcal vaccine-induced cellular immune responses in post-traumatic splenectomized individuals. Journal of clinical immunology, 37(4), 388-396.Özet
Splenectomy is associated with increased risk of overwhelming post-splenectomy infections despite proper anti-pneumococcal vaccination. As most studies concentrated on vaccination-induced humoral immunity, the cellular immune responses triggered in splenectomized patients are not yet well studied. The present study aims to investigate this area as it can contribute to the development of more effective vaccination strategies.Five healthy and 14 splenectomized patients were vaccinated with pneumococcal conjugate polysaccharide vaccine (PCV) followed by pneumococcal polysaccharide vaccine according to the guidelines established by Advisory Committee on Immunization Practices. PBMC samples collected 0, 8, and 12 weeks after PCV immunization were in vitro stimulated with PCV. Levels of lymphoproliferation, T-H cell differentiation, and cytokine release were assessed by carboxyfluorescein succinimidyl ester labeling, intracellular cytokine staining, and ELISA, respectively.While T(H)1-dominated immune response was detected in both groups, asplenic individuals generated significantly lower levels of T(H)1 cells following in vitro stimulation. Similarly, levels of IFN-gamma, IL-4, and IL-17 release and lymphoproliferation were significantly lower in asplenic patients.According to our data, splenectomy negatively influences the levels of PCV-induced lymphoproliferation, T(H)1 differentiation, and cytokine release. Besides, PCV failed to induce T(H)17-dominant immune response which is crucial for protection against extracellular pathogens.
Kaynak
Journal of Clinical ImmunologyCilt
37Sayı
4Koleksiyonlar
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