Autoimmune diseases, allergies and chronic inflammations affect about 2-15% of the world population, with rising prevalences, high healthcare burdens and socio-economic impacts costing hundreds of billion dollars annually (Miller FW, Curr. Opin. Immunol., 2023).
The 2025 Nobel Prize for Medicine, awarded to Prof M. Brunkow, Prof F. Ramsdell, and Prof S. Sakaguchi for their discovery of peripheral immune tolerance by regulatory T cells, highlights the critical role of the immune tolerance mechanism that was embedded in the human immune system to protect us from autoimmune diseases, allergies, GvHD, transplant rejections, and other chronic inflammatory conditions. The manifestations of chronic inflammation in these conditions typically arise from an imbalance between autoreactive inflammatory and immune tolerance responses of the host.
Despite significant advances in treatments achieved with mAb biologics and small molecule inhibitors, between 10- 50% of patients will fail to respond or eventually developed resistance to current treatments. The current therapeutic paradigm and strategies primarily targets suppression of inflammation by blocking pro-inflammatory cytokines or intracellular signaling pathways without addressing the immune tolerance side of the equation to address the key underlying cause of diseases. These treatments also pose serious risks of infections and immuno-compromises due to a broad immunosuppression as a lifelong medication. The current clinical challenges represent a significant unmet patient need. An ideal therapy should aim to induce or rebalance immune tolerance responses without compromising the host’s immune defense.
Anti-IgD monoclonal antibody (mAb) is a first-in-class, disease-modifying therapeutic mAb that binds to immunoglobulin D (IgD) expressed on B cells to activate the immune responses to engage our body’s inbuilt regulatory immune tolerance mechanisms and anti-inflammatory responses to address the underlying causes of human autoimmune diseases, allergies and chronic inflammations.
Distinctively different from the current treatments with immunosuppressants, anti-IgD mAb is designed to activate a particular immune response, rather than suppressing it, to engage and harness our body’s inbuilt immune tolerance mechanisms and regulatory feedback anti-inflammatory responses. Anti-IgD mAb restores the balances between the immune tolerance and pro-inflammatory states by activating regulatory T cells and regulatory B cells, inducing anergic and regulatory phenotypes in B cells, selectively depleting harmful IgD+ mature B cells, and promoting an anti-inflammatory Th2-leaning response to deliver a long last therapeutic effect with minimal compromises to the host’s protective immunity against infections (Nguyen TG, Int. Rev. Immunol., 2022).
IMT aims to develop anti-IgD mAb as an innovative, paradigm shifting, and disease modifying mAb treatment for human chronic inflammations including autoimmune diseases, allergic conditions, graft versus host diseases (cGVHD), organ transplant rejections, chronic obstructive pulmonary diseases (COPDs), and potentially Alzheimer’s and Parkinson’s diseases. IMT also intends to design anti-IgD mAb as a platform adaptable to other potential modalities.
The preclinical proof of concept of anti-IgD mAb originated from postdoctoral research works and discoveries by IMT Chief Scientific Officer and Founder, Dr Tue (Tommie) Gia Nguyen, demonstrating the novel therapeutic efficacies, safety and modes of action (MoA) of anti-IgD mAb in clinically relevant mouse models of rheumatoid arthritis, atopic and allergic contact dermatitis. These findings on therapeutic efficacies and MoA of anti-IgD mAb have been recently confirmed and corroborated by other independent studies in various mouse models of other autoimmune and allergic conditions. The peer-reviewed publications and corroborating evidence relevant to anti-IgD mAb technology are available on IMT Research Publications link.
IgD Mab Technology (IMT) 