Genorise Recombinant Canine IL-14A (TXLNA) Summary

Alternative names for IL-14A: Interleukin 14 alpha, IL14A, TXLAN, alpha-taxilin

Alternative name for canine: Dog

Product Specifications

Background: 

Interleukin-14 alpha (IL-14A), also known as alpha-taxilin (encoded by the TXLNA gene) [1], is a high-molecular-weight B-cell growth factor (HMW-BCGF) that promotes the proliferation of normal and cancerous B-cells [2]. It is involved in immune responses and is implicated in the pathogenesis of autoimmune diseases like SLE and Sjogren’s syndrome. IL-14A induces B-cell proliferation, inhibits antibody secretion by inhibiting differentiation into antibody-secreting plasma cells, and expands selected B-cell subgroups. IL-14A is involved in Ca2+-dependent exocytosis in neuroendocrine cells [3]. This interleukin is produced mainly by T cells and certain malignant B cells. IL-14A has significant clinical value as a predictive biomarker and a key mediator in autoimmune disease pathogenesis. Serum levels of IL-14α can serve as a biomarker to monitor responses to immunotherapy in patients with advanced solid cancers. IL-14α is considered a putative biomarker for the stratification and diagnosis of Sjögren’s disease (SjD) and related dry eye conditions. Patients with primary and secondary Sjögren’s syndrome express significantly higher levels of IL-14α in their peripheral blood compared to healthy individuals. Elevated levels are found in aggressive B-cell non-Hodgkin’s lymphoma, Sjögren’s syndrome, and Systemic Lupus Erythematosus (SLE). Early changes in serum IL-14α levels (measured after two cycles of anti-PD-1 therapy like pembrolizumab) can predict patient survival and treatment response. While the precise nature of interleukin-14 remains under study, the alpha subunit has been identified as a critical factor in the development of B-cell-related disorders.

References

1. Nogami S, et al. (2004). Biochem. Biophys. Res. Commun. 319 (3): 936–43.
2. Ambrus JL, et al.(1993). Proc. Natl. Acad. Sci. U.S.A. 90 (13): 6330–4.
3. Nogami S, et al. (2003). Genes Cells. 8 (1): 17–28.