CD19 Deficiency Leads to Dysregulation of Phosphoinositide 3-Kinase-Protein Kinase B (PI3K/AKT) and Nuclear Factor Kappa B (NF-κB) Pathways: Implications for B-Cell Maturation and Immune Function

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dc.contributor.authorKüçcüktürk, Serkan
dc.contributor.authorKaraselek, Mehmet Ali
dc.contributor.authorDuran, Tugce
dc.contributor.authorReisli, Ismail
dc.date.accessioned2025-04-30T12:39:12Z
dc.date.available2025-04-30T12:39:12Z
dc.date.issued2025
dc.departmentKMÜ, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü
dc.description.abstractObjective: CD19 is a cellular receptor belonging to the immunoglobulin (Ig) superfamily and serves as a critical signaling component in B-cells differentiation and activation. This study investigates gene expression changes in the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) pathways in patients with CD19 deficiency. The role of CD19 in B-cell function was explored, along with its potential impact on these signaling pathways and the overall immune response. Materials and Methods: RNA samples were obtained from three patients diagnosed with CD19 deficiency, as well as heterozygous carriers and healthy controls. Gene expression profiles related to the PI3K/AKT axis and NF-kappa B pathway were analyzed using quantitative polymerase chain reaction (PCR). Results:The study revealed significant alterations in the expression of signaling pathway components, including PI3K, phosphoinositide-3-kinase regulatory subunit 1 (p85),TNF receptor-associated factor 2 (TRAF2), forkhead box O1 (FOXO1), and NF-kappa B, in CD19deficient patients. While PI3K and NF-kappa B expression were significantly downregulated in these patients, CD19, p85, FOXO1, and TRAF2 expression were markedly upregulated. These changes suggest impaired B-cell function, leading to weakened immune system responses. Conclusion: CD19 deficiency disrupts B-cell receptor signaling, resulting in significant alterations in the PI3K/AKT axis and NF-kappa B pathways. These disruptions impair B-cell maturation and survival, ultimately leading to compromised immune responses. This study provides the first detailed molecular insights into the effects of CD19 deficiency, enhancing our understanding of how these signaling pathways regulate immune function.
dc.identifier.doi10.14744/cpr.2025.73280
dc.identifier.endpage118
dc.identifier.issn2980-2156
dc.identifier.issue2
dc.identifier.startpage111
dc.identifier.urihttps://doi.org/10.14744/cpr.2025.73280
dc.identifier.volume47
dc.identifier.wosWOS:001466117800002
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.institutionauthorKüççüktürk, Serkan
dc.institutionauthoridKüçcüktürk, Serkan/0000-0001-8445-666X
dc.language.isoen
dc.publisherErciyes Üniv Sch Medıcine
dc.relation.ispartofJournal Of Clinical Practıce And Research
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectB cell maturation
dc.subjectCD19 deficiency
dc.subjectimmune responses
dc.subjectnuclear factor kappa B (NF-kappa B)
dc.subjectphosphoinositide 3-kinase-protein kinase B (PI3K/AKT) axis
dc.titleCD19 Deficiency Leads to Dysregulation of Phosphoinositide 3-Kinase-Protein Kinase B (PI3K/AKT) and Nuclear Factor Kappa B (NF-κB) Pathways: Implications for B-Cell Maturation and Immune Function
dc.typeArticle

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