Evaluation of the T Helper 17 Cell Specific Genes and the Innate Lymphoid Cells Counts in the Peripheral Blood of Patients With the Common Variable Immunodeficiency



Ganjalikhanihakemi M^{1, 2} ; Yazdani R³ ; Sherkat R⁴ ; Homayouni V² ; Masjedi M² ; Hosseini M⁵
Source: Journal of Research in Medical Sciences Published:2014

Abstract

Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran Department of Biostatistics and Epidemiology, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran Background: Common variable immunodeficiency (CVID) is characterized by a deficiency in the immune system with a heterogeneous collection of disorders resulting in antibody deficiency and recurrent infections. T helper 17 (Th 17) cells promote B-cell survival and synergize with the B-cell activating factor to induce their differentiation into the plasma cells. A sub-population of innate lymphoid cells (ILCs) also produces interleukin 17 (IL-17). Th is study aimed to measure the Th 17 specific genes and ILCs counts in the CVID patients in comparison with control subjects. Materials and Methods: Total messenger ribonucleic acid (mRNA) was extracted from the whole blood samples of 10 CVID patients and 10 healthy individuals. IL-17, retinoic acid receptor-related orphan receptor C2 (RORC2), IL-23R, and IL-9 gene expression were measured using the quantitative reverse transcriptase-polymerase chain reaction. Count of lineage negative/CD127+/CD90+ ILCs in the blood samples was performed by the flow cytometry method. Results: The transcript levels of IL-17 and RORC2 in CVID patients was strongly lower than control subjects (P = 0.049 and P = 0.046, respectively), but slight reduction in the IL-23R expression (P = 0.252) have seen in the CVID patients. Accordingly, the number of ILCs decreased significantly (P = 0.04). Interestingly, IL-9 mRNA level was more significantly in the CVID patients (P = 0.001). Conclusion: The results presented in this study show that the Th 17 cell specific genes expression (as the determiner Th 17 cells) and ILCs (another lymphoid source of IL-17) are decreased in patients with CVID and this could be an explanation for the defect of their humoral immune response. In addition, elevation of the IL-9 gene expression may shed a new light into the way toward the understanding of the mechanism of autoimmunity in the CVID patients.