BTLA Specific Neutra™ Antibody Products

BTLA (B and T Lymphocyte Associated) stands as a constituent of the immunoglobulin superfamily, acting as a receptor transmitting inhibitory cues to attenuate immune reactions. Genetic variations within this gene have been linked to heightened susceptibility to rheumatoid arthritis. Conditions linked to BTLA encompass rheumatoid arthritis and arthritis. The intricate routes of BTLA traverse through the domain of the innate immune system and the processing and presentation of antigens mediated by Class I MHC molecules.

Its Gene ID: 151888, UniProtKB ID: Q7Z6A9, and OMIM ID: 607925.

BTLA Signaling Pathway

BTLA functions as an immune-regulatory receptor predominantly expressed across B-, T-, and mature lymphocyte cells. Upon interaction with the Herpes virus entry mediator (HVEM) displayed by APCs, BTLA orchestrates downstream signaling pathways. These pathways associated with BTLA, regardless of whether they stimulate or inhibit, exert control over the progression of HBV-ACLF, hepatocellular carcinoma, liver cirrhosis, and graft acceptance and rejection. Inhibiting the BTLA signaling cascade hampers T-cell functionality, promotes immune system recognition of cancer cells, and facilitates tumor clearance. Strategies applying blockade of the HVEM-BTLA signaling axis have emerged as novel anticancer modalities, ushering in a wave of anticancer therapeutics aimed at BTLA.

Fig.1 BTLA-associated signaling pathways.^{1, 2}

BTLA Antibodies Applications

• Anti-BTLA mAb Modulates T Cell Responses

BTLA, classified within the cohort of co-inhibitory receptors, is a member of the CD28 immunoglobulin superfamily. Through the utilization of monoclonal antibodies (mAbs) targeting human BTLA, its constitutive presence is observed on the majority of CD4⁺ and CD8⁺ T cells, with its expression gradually diminishing following T cell activation. Both BTLA-positive and BTLA-negative subsets are found within polarized Th1 and Th2 cells, yet prolonged cultivation leads to a reduction in BTLA expression. Activation of BTLA through cross-linking with an agonistic mAb suppresses T cell proliferation and the generation of IFN-γ and IL-10 cytokines upon anti-CD3 stimulation. The inhibition of T cell activation mediated by BTLA operates during primary CD4⁺ T cell responses and secondary CD4⁺ and CD8⁺ T cell responses, indicating that BTLA engagement transmits a persistent "off" signal to T cells, potentially contributing significantly to the preservation of T cell tolerance.

• Harnessing Anti-BTLA Antibodies for CHS Therapy

Assessing the therapeutic viability of an activating agent targeting BTLA in contact hypersensitivity (CHS), the impact of an activating anti-BTLA antibody on CHS has been investigated. In vivo administration of the anti-BTLA antibody mitigates DNFB-triggered CHS and reduces the production of IFN-γ by CD8⁺ T cells. These findings imply that activation of BTLA with agonistic agents holds promise as a therapeutic approach for CHS.

Creative Biolabs presents over 10 intricately designed anti-BTLA antibodies, crafted through advanced recombinant methodologies. Furthermore, bespoke tailoring services are available for tailoring neutralizing antibodies aimed at BTLA to exacting specifications.

REFERENCES

1. Yu, Xueping, et al. "BTLA/HVEM signaling: milestones in research and role in chronic hepatitis B virus infection." Frontiers in immunology 10 (2019): 431156.
2. Distributed under Open Access license CC BY 4.0, without modification.