Read the Peer-Reviewed Science Backing Our Treatment

In this key work which expounds upon numerous publications, including Decker et al (2009), it is shown that this unique and powerful intrinsic Dendritic Cell mechanism is regulated down the level of the specific amino acid sequences being bound to both MHC Class I and II, that they must be bound to MHC Class I and II simultaneously, and that the sequences must match entirely to generate this powerful Th1 immune response.

A change of even a couple of amino acids to eliminate the ‘100% overlap’ completely eliminates the response, demonstrating how fine-tuned and important this biological feat is. Unique to this ‘overlapped’ mechanism of Dendritic Cell loading is the downstream secretion of a powerful Th1 immune promoter, AIMp1 (a.k.a. p43) and the statistically significant upregulation of antigen-specific Killer T cells in circulation.

These results are repeatedly and eloquently shown through various experiments within this publication, and importantly it is also shown that other stimuli often used with Dendritic Cell or immunotherapy attempts (e.g., TLR agonists, bacterial components, viral components, interferons) were unable to replicate these responses, even when combined. The specific intracellular complex responsible for comparing MHC Class I and II bound sequences is also studied and demonstrated to be involved and critical.

Taken together, the findings published here are the detailed underpinnings of the mechanism driving the unique and powerful Dendritic Cell technology employed by Immunocine.

This work continues to build exponentially on previous published works by showing the importance of ‘overlapped’ loading in Dendritic Cells in a mouse model of pancreatic cancer. Continued study has revealed that the Dendritic Cells are able to immune-attack a wide range of targets if loaded in this way, regardless of where or what the target may be.

It is shown here that this type of immunotherapy (a.k.a. Dendritic Cell ‘overlapped’ loading with a target) can combine effectively with standard of care cancer treatments (e.g., chemotherapy), that the results are target-specific, and that the combination leads to significantly better treatment outcomes.

Importantly, it is thoroughly demonstrated that a truly unique population of memory T cells are propagated from this type (and only this type) of Dendritic Cell therapy, and that this greatly reduces the risk of relapse (as shown within the publication) and carries significant long-term protection capabilities.

Taken together, it has been shown that this powerful, specific, and special Th1 immune response has numerous unique outcome measures, is able to be translated from laboratory findings to preclinical successes in even very difficult to treat cancer models, and may in fact have strong utility in the future global treatment approach for cancer.

This publication specifically focuses in on the unique set of Killer and Memory T cells which seem to originate only from Dendritic Cells loaded with the Immunocine protocol. This work dives into the natural genetic reprogramming of the T cells, what allows for their long-term memory, and how they are able to be so improved at killing target cells (e.g., cancer cells). Not only are these cells shown to be superior at cancer killing, but they continue to elucidate how the Immunocine Dendritic Cell treatment is unique, specific, and more powerful than other Dendritic Cell attempts which do not lead to the proliferation of these T cells. Taken together, the entire Immunocine cellular pathway from education (Dendritic Cells) to effectiveness (unique Killer T cells) is being mapped out and understood to a level which allows for meticulous care in treatment and safety.

This is a case report of a patient treated with Th1-empowered Dendritic Cells, in which remission was observed. Long-term remission was maintained at last follow-up.

This is a case report of a patient treated with Th1-empowered Dendritic Cells, in which remission was observed. As of 2022, this patient is still alive.

This canine trial was focused on extrapolating the results of the powerful Th1-empowered Immunocine Dendritic Cells from the lab to the clinic in real-world cases and attempted to overcome the most aggressive cancer simply known to exist – canine splenic hemangiosarcoma (median survival of 48 days, 100% lethal).

Though not every dog was “cured,” 40% showed significant improvement including an example of long-term remission with no cancer identified at time of autopsy (death due to old age). These results provide preliminary evidence of the utility of this science in real cases, and suggests further study and use is extremely warranted.

This Phase I study found that the double-loaded dendritic cell treatment could be safely combined with standard glioblastoma care and produced signs of durable T-cell activation in both the blood and tumor, alongside encouraging early survival.

This peer-reviewed study provides encouraging clinical support for the approach used at Immunocine. Five patients with advanced cancers—including melanoma, breast, prostate and bladder cancer—who had already failed standard treatments were treated with Immunocine’s personalized dendritic cell therapy, and all five achieved complete or near-complete remissions that were ongoing for as long as 28 months. Importantly, the dendritic cells were “double loaded” in simultaneous fashion with two forms of information from each patient’s own tumor: tumor mRNA and tumor lysate. This is designed to not only allow the dendritic cells to show the immune system a broader picture of the cancer through both major antigen-presentation pathways, but also to launch a unique and powerful Th1 immune response against their respective targets. While this small case series does not prove that double loading is superior or establish the treatment’s overall effectiveness, it provides real-world, peer-reviewed evidence that Immunocine’s double-loaded approach can generate deep and durable responses in some patients with very difficult-to-treat cancers and supports its continued study in larger efforts.

This publication exhaustively demonstrates that Dendritic Cells possess the immune suppressor CTLA-4 and normally secrete this molecule to reduce inflammation.

In a variety of publications presented here, it is shown that Th1 ‘overlapped’ Dendritic Cells reduce their CTLA-4 expression and secretion and this leads to stronger anti-cancer immune responses. This publication was highlighted on the cover of the journal.

This set of studies demonstrates the power of a recently discovered Th1-promoting molecule, AIMp1 (a.k.a. p43), and in fact shows that often Th1 immune responses are completely lacking if AIMp1 is absent.

Cancer patients which spontaneously have higher levels of AIMp1 survive longer against cancer than patients deficient in AIMp1, and actually have a larger differential importance than Interferon-𝛾, as is shown within this publication.

Numerous publications herein clearly outlay that Dendritic Cells loaded with the Immunocine ‘overlapped’ protocol abundantly secrete and use AIMp1 to promote this uniquely powerful and specific Th1 anti-cancer response, while other Dendritic Cell or immunotherapy approaches fail to promote this effect.

This review explains how the mARS complex acts as an immune-regulatory sensor within dendritic cells and how release of AIMp1 can promote the strong Th1 immune responses needed to fight cancer.

Cancer does more than simply grow—it actively creates defenses that can make it difficult for the immune system to recognize and attack it. In this research, we showed in several aggressive laboratory models that attacking those defenses from multiple directions could dramatically change the environment around the tumor, allowing the immune system to become much more active. Treatment increased cancer-fighting immune cells, reduced some of the cells and signals that normally suppress immunity, and even produced lasting immune memory capable of recognizing cancer elsewhere in the body. Although this study was not specifically testing Immunocine’s current dendritic cell therapy, the lessons learned from this work continue to influence how we think about cancer treatment: generating a robust immune response is great—but we also want to look for ways to create conditions in and around the tumor that allow that response to succeed. These principles continue to help us evolve Immunocine’s strategies toward increasingly comprehensive, physiologically guided ways of helping a patient’s own immune system recognize and attack cancer.

This study shows that overlapping MHC Class I and Class II antigen loading reprograms dendritic cells into a powerful, cDC1-like state specialized for activating cancer-fighting T cells. It identifies reduced mTORC1 signaling, increased IL-12, and decreased IL-10 as key parts of this response.

This study found that tumors containing more CD8⁺CD161⁺ T cells were associated with longer survival, stronger cancer-killing activity, and less T-cell exhaustion—and that this benefit appeared to depend on dendritic cells.