Hearing restoration and the stria vascularis: evidence for the role of the immune system in hearing restoration

Samaha, Nadia Lara; Almasri, Mohamad; Johns, J. Dixon; Hoa, Michael

doi:10.1097/moo.0000000000000738

Cited by 3 publications

(2 citation statements)

References 93 publications

(149 reference statements)

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“…There is growing evidence of the involvement of the immune system, particularly T-lymphocytes and specific autoimmune reactive antibodies ( 28 ). Humoral and cell-driven responses cause susceptible antigen-presenting cells (B and T-cells) to produce autoantibodies toward tissues involved in the auditory pathway when interleukin-17, interferon-gamma, and tumor necrosis factor are expressed ( 12 ). Ben-Sasson SZ et al confirmed that the cytokine IL-1 can enhance the antigen-driven response of CD4 and CD8 T cells ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

“…An increasing amount of research indicates that immune-associated processes may play essential role in deafness as well as mechanisms involving autoimmune and autoinflammatory diseases may also affect hearing. For example, autoimmune inner ear disease ( 8 ), Meniere’s disease ( 9 ), Cogan’s syndrome ( 10 ), and NLRP3-related autoinflammatory diseases ( 11 ) have been found to be strongly associated with SSHL ( 12 ). Research findings indicate that elevated antibody levels may lead to the condition through indirect reactions with internal hearing antigens or stimulated T-cells.…”

Section: Introductionmentioning

confidence: 99%

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Causal role of immune cell phenotypes in idiopathic sudden sensorineural hearing loss: a bi-directional Mendelian randomization study

Li,

Zhou,

Zhou

et al. 2024

Front. Neurol.

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BackgroundA growing body of evidence suggests that immunological processes have a significant role in developing idiopathic sudden sensorineural hearing loss (SSHL). However, few studies have examined the association between immune cell phenotype and SSHL using Mendelian Randomization (MR).MethodsThe online genome-wide association studies (GWAS) database was used to compile data from GWAS covering 731 immunophenotypes and SSHL. Inverse variance weighted (IVW) analysis was primarily used for MR study, and single nucleotide polymorphisms (SNPs) associated with immunophenotypes served as dependent variables. A sensitivity study and the false discovery rate (FDR) correction were used to examine the MR hypothesis. In addition, the possibility of reverse causality between immunophenotype and SSHL was validated by reverse MR. Reverse MR was analyzed in a manner consistent with forward MR.ResultsAfter FDR correction and sensitivity analysis, we screened 7 immunophenotypes, including IgD+ CD38dim %lymphocyte (95% CI: 1.0019, 1.0742, p = 3.87 × 10−2, FDR = 1.15 × 10−2); Unsw mem AC (95% CI: 1.004, 1.2522, p = 4.23 × 10−2, FDR = 2.25 × 10−2); CD86+ myeloid DC AC (95% CI: 1.0083, 1.1147, p = 2.24 × 10−2, FDR = 4.27 × 10−2); CD33dim HLA DR− AC (95% CI: 1.0046, 1.0583, p = 2.12 × 10−2, FDR = 4.69 × 10−2); SSC-A on CD8br (95% CI: 1.0028, 1.1461, p = 4.12 × 10−2, FDR = 4.71 × 10−2); CD45RA− CD4+ %T cell (95% CI: 1.0036, 1.0503, p = 2.32 × 10−2, FDR = 4.82 × 10−2); DP (CD4+CD8+) AC (95% CI: 1.011, 1.2091, p = 2.78 × 10−2, FDR = 4.97 × 10−2). There was a strong causal relationship with SSHL onset, and the reliability of the results was verified. Furthermore, the immunological cell profile and SSHL did not appear to be closely associated, as shown by reverse MR analysis.ConclusionOur study provides more support for the current hypothesis that immunophenotypes and the pathophysiology of SSHL are closely associated. Further validation is needed to assess the role of these immunophenotypes in SSHL.

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Section: Discussionmentioning

confidence: 99%