MICB Specific Neutra™ Antibody Products

MICB (MHC class I polypeptide-related sequence B) is a protein encoded by the MICB gene in humans. It belongs to the MHC class I family, sharing structural similarities with classical MHC class I molecules. MICB contains α1, α2, and α3, three extracellular domains. It functions as a stress-induced ligand for the activating immune receptor NKG2D. MICB's interaction with NKG2D helps in immune surveillance against infected or malignant cells.

Its Gene ID: 4277, UniProtKB ID: Q29980, and OMIM ID: 602436.

MICB Activation

MICB activation primarily occurs through stress induction mechanisms, such as cellular infection, transformation, or other forms of cellular stress. After activation, MICB expression is regulated by various cellular processes involving cytokines, such as interferons, tumor necrosis factor-alpha, and other stress-inducing factors to promote MICB upregulation. Once expressed, MICB engages with the NKG2D receptor on immune cells, including NK cells, γδ T cells, and CD8⁺ T cells, leading to their activation. The binding of MICB to NKG2D triggers downstream signaling pathways, leading to the activation of immune cells and subsequent elimination of stressed or infected cells.

MICB Function

MICB plays a crucial role in immune surveillance and immune response regulation. It participates in the recognition and elimination of stressed or infected cells by engaging with the NKG2D receptor. This interaction triggers cytotoxic responses, such as the release of perforin and granzymes, leading to the destruction of target cells. Dysregulation of MICB expression and NKG2D signaling has been implicated in various diseases, including cancer, autoimmune disorders, and viral infections. In cancer, downregulation of MICB expression allows tumors to evade immune surveillance. Strategies to regulate MICB expression in cancer therapy include targeting pathways involved in its transcriptional regulation or using immunotherapeutic approaches to enhance MICB expression. In autoimmune diseases, aberrant MICB expression may contribute to the activation of autoreactive immune cells, leading to tissue damage and inflammation. Therapeutic interventions targeting MICB-NKG2D interactions or modulating MICB expression levels could potentially alleviate autoimmune pathology.

Fig.1 Dual role of MICB in immunosurveillance by NK cells and tumor immune escape.¹

Antibodies Targeting MICB

Therapeutic antibodies targeting MICB serve as an innovative model for immunotherapy. Antibody-mediated targeting of the MICB could specifically inhibit MICB proteolytic shedding. Antitumor immunity is primarily mediated by NK cells via activating NKG2D and CD16 Fc receptors. This method prevents tumors from losing critical immunostimulatory ligands while also reactivating anticancer immunity. Studies have found that these antibodies can induce antibody-dependent cellular cytotoxicity or complement-dependent cytotoxicity against MICB-expressing tumor cells, leading to their elimination by immune cells. Additionally, these antibodies are demonstrated to suppress tumor development in totally immunized mouse models and inhibit melanoma metastases in a humanized mouse model. By targeting MICB, these therapeutic antibodies offer promising strategies for enhancing immune surveillance and reducing tumor burden or autoimmune pathology.

Fig.2 Therapeutic opportunity for anti-MICA/B antibody.¹

Creative Biolabs offers anti-MICB antibody products used for several applications. These antibodies are produced recombinantly, ensuring high batch-to-batch consistency and long-term supply security.

REFERENCE

1. Fuertes, Mercedes Beatriz, Carolina Inés Domaica, and Norberto Walter Zwirner. "Leveraging NKG2D ligands in immuno-oncology." Frontiers in Immunology 12 (2021): 713158. Distributed under Open Access license CC BY 4.0, without modification.