The Real Race to Cure Type 1 Diabetes: Inside the New Era of Cell and Immune Therapies
For decades, people with type 1 diabetes (T1D) have been told a familiar truth: their immune system mistakenly attacks the pancreas, destroying insulin-producing beta cells. Without those cells, the body can’t control blood sugar, and insulin injections become a lifelong requirement.
But something extraordinary is happening. For the first time, scientists aren’t just trying to manage blood sugars — they’re working to cure the disease at its biological root.
Two major approaches are taking shape:
Cell therapies, which aim to replace the insulin-making cells that were lost, and
Disease-modifying therapies, which aim to retrain the immune system to stop attacking the pancreas in the first place.
Some of these advances are already approved by the FDA; others are in clinical trials that could change what it means to live with T1D in the next few years.
Let’s break down what’s happening — in plain language.
1. Cell Therapies: Replacing What Was Lost
The idea
The simplest way to think about cell therapy is this: instead of giving the body insulin from a vial or pump, give it back the cells that make insulin naturally.
That’s the promise of islet cell transplantation — infusing living clusters of pancreatic cells that sense blood sugar and release insulin on demand.
The goal isn’t just to lower blood sugar. It’s to restore the natural, automatic regulation that non-diabetic people take for granted.
The first approved cell therapy: Lantidra ®
In 2023, the FDA approved the first cell-based therapy for T1D, called Lantidra (donislecel). It’s a major milestone — the first time the agency has said “yes” to replacing lost insulin-producing cells.
Lantidra is made from donor islets — real pancreatic cells taken from deceased organ donors, purified, and infused into a patient’s liver. Once inside the body, these cells can start releasing insulin when blood sugar rises.
Lantidra is approved for adults with T1D who experience severe, repeated low blood sugars despite best medical care. For many of these patients, it can reduce or even eliminate the need for injected insulin — sometimes for years.
However, there’s a catch: because the transplanted cells come from another person, the immune system sees them as foreign. Patients must take immunosuppressive drugs for life to prevent rejection. These medicines weaken the immune system and can have side effects, so the therapy is currently limited to those who face serious risks from hypoglycemia.
Still, Lantidra’s approval proves the concept — that islet cell replacement works. Now the field is racing to make it safer, more durable, and accessible to everyone with T1D.
Donor-derived vs. Manufactured Islets: What’s the Difference?
Donor-derived islets (like those used in Lantidra) come from human pancreas donors. They work very well — these are real human cells, after all — but donor supply is scarce. Only a few thousand pancreases are available per year, far fewer than the millions of people who could benefit.
That’s why many scientists have turned to manufactured islets — insulin-producing cells made from pluripotent stem cells in the lab. These stem cells can be grown indefinitely and coaxed into becoming fully functional islet-like clusters.
Companies like Vertex Pharmaceuticalsare leading this work. Vertex recently reported that some patients who received its stem-cell-derived islets regained the ability to make their own insulin, with measurable C-peptide levels (a marker of natural insulin production). In some cases, insulin needs dropped by more than 90%.
That’s remarkable — and it’s only the beginning. Because these cells are lab-made, they can also be engineered for safety and protection.
The Double Challenge: Two Immune Attacks
Even if we successfully replace the beta cells, there’s still a problem. The new cells face two kinds of immune attack:
Rejection, because the body recognizes donor or lab-made cells as foreign.
Autoimmunity, the same self-directed immune attack that caused diabetes in the first place.
Both must be solved for a durable cure. That’s where innovation around immune protection comes in.
Protecting the New Cells: Three Key Strategies
1. Encapsulation – building a physical shield
Imagine wrapping the new beta cells in a microscopic suit of armor that lets nutrients and insulin flow freely, but keeps out immune cells and antibodies. That’s the idea behind encapsulation.
Encapsulation devices can take many forms — tiny capsules, flat membranes, or small pouches implanted under the skin. The goal is to create a “home” where cells can thrive while being invisible to the immune system.
Several clinical trials have tested encapsulated islet devices, and while results have varied, newer designs have shown both safety and insulin secretion for up to a year. The key challenge is maintaining oxygen and nutrient flow so the cells stay alive long-term — something researchers are improving with each iteration.
2. Local Immune Modulation – creating a peaceful neighborhood
Instead of using systemic drugs that suppress the entire immune system, scientists are experimenting with ways to calm the immune environment right around the transplanted cells.
One example is local immune modulation, where the implant itself releases small amounts of immune-calming molecules or is coated with anti-inflammatory compounds. Think of it as turning the local immune “temperature” down to prevent an attack without affecting the rest of the body’s defenses.
Researchers are also testing ways to deliver “regulatory” immune cells alongside the graft to teach the immune system that these new cells are safe.
3. Gene Editing – making cells invisible
The newest frontier is to use gene editing tools like CRISPR to make replacement cells that are invisible to the immune system.
By deleting or altering certain cell-surface proteins that trigger rejection or adding protective ones that send “don’t attack” signals, scientists can make cells that avoid immune destruction.
These “hypoimmunogenic” (meaning they lay low) or “stealth” cells are already being tested in animals and are moving into human studies. If successful, they could eliminate the need for lifelong immunosuppression — the biggest barrier to widespread use!
But, how Close Are We?
We now have:
One FDA-approved donor islet therapy (Lantidra) for a specific patient population.
Several stem-cell–derived islet products in advanced clinical trials showing real insulin production.
Next-generation encapsulation devices and gene-edited cells entering human studies.
This progress means the first broadly available, durable cell therapies for T1D could realistically arrive within the next few years — no longer decades.
2. Disease-Modifying Therapies: Reprogramming the Immune System
While cell therapy replaces lost cells, disease-modifying therapy aims to stop the immune attack altogether.
The immune system in T1D behaves like an overzealous security guard, mistaking the pancreas’s beta cells for intruders. Disease-modifying therapies work by retraining or calming this immune response — ideally before too much damage is done.
The First FDA-Approved Immune Therapy: Teplizumab
In 2022, the FDA approved Teplizumab (Tzield), a monoclonal antibody that binds to CD3 on T cells — the white blood cells that destroy beta cells.
In people with early-stage T1D (those who already have autoantibodies but normal blood sugars), teplizumab was shown to delay the onset of clinical diabetes by about two years on average. Some participants remained diabetes-free for much longer.
It’s not a cure, but it’s the first proof that we can change the course of the disease itself — by rebalancing immunity before full diabetes develops.
How Scientists Are Trying to “Reeducate” the Immune System
Researchers are exploring several complementary ways to modify the immune attack.
a) Disabling autoreactive cells
Teplizumab is the best-known example, but others are in development. Some therapies remove or inactivate specific immune cells (like T or B cells) that recognize beta-cell antigens. Others block inflammatory signals that increase the attack.
b) Enhancing immune regulation
The immune system has “peacekeeper” cells called regulatory T cells (Tregs) that prevent excessive immune reactions. In T1D, these cells often don’t work well enough.
Several studies are testing ways to expand or strengthen Tregs — for example, by taking a patient’s own Tregs, growing them in the lab, and infusing them back. The hope is to restore immune balance naturally, without heavy immune suppression.
c) Reducing inflammation and protecting beta cells
Some therapies focus on the environment rather than the immune cells themselves. Chronic inflammation and metabolic stress make beta cells more vulnerable to destruction. By calming inflammation or shielding beta cells from stress, researchers hope to preserve what remains — or even help them regrow.
Regenerating and Expanding Beta Cells
Interestingly, even years after diagnosis, some people with T1D still have a few surviving beta cells. Scientists are exploring how to protect and expand these.
Certain molecules (like DYRK1A inhibitors or GLP-1–based compounds) can coax beta cells to divide or improve their survival. Combining these regenerative drugs with immune therapies could lead to partial restoration of insulin production — a “functional cure” where people need little or no insulin.
The Future: Combining Both Strategies
Most experts now believe the ultimate solution will be a combination of cell therapy and immune therapy.
For people early in the disease: immune therapy may delay or prevent diabetes altogether.
For those with established diabetes: immune protection paired with cell replacement could offer true insulin independence.
Researchers are already testing combinations — for example, pairing gene-edited stem-cell islets with short-term immune modulation, or giving teplizumab before a cell transplant to reduce rejection risk.
These layered strategies recognize that T1D is both a cell-loss problem and an immune problem. To cure it, we’ll need to fix both.
What’s Approved and What’s Coming
Approved Today
Teplizumab (Tzield): delays onset of T1D in at-risk individuals.
Lantidra (donislecel): replaces insulin-producing cells for adults with severe hypoglycemia.
In Late-Stage Trials
Stem-cell–derived islets (Vertex VX-880 and VX-264) — human proof-of-concept achieved; pivotal trials underway.
Encapsulation devices that may allow implantation without immunosuppression.
Gene-edited hypoimmunogenic islets entering early human testing.
Treg and IL-2–based immune therapies showing early promise for restoring immune balance.
What This Means for Patients
If you live with T1D, you already know what it means to manage the disease every day — constant glucose checks, carb counts, insulin adjustments.
Now imagine a future where your body senses and controls blood sugar naturally again. That’s no longer science fiction. It’s science in progress.
It’s important to stay grounded: not every therapy will be right for everyone, and safety must come first. But we are closer than ever to therapies that don’t just treat blood sugar — they change the biology of the disease.
If you’re interested in these advances, ask your endocrinologist about:
Clinical trials in your area
Eligibility for immune therapy screening (especially for relatives of people with T1D)
Updates from reputable organizations like Breakthrough T1D and the NIH
The next few years will likely bring more firsts: the first immune combination therapy, the first encapsulated implant without immunosuppression, maybe even the first durable insulin independence for people who’ve had diabetes for decades.
The race to cure type 1 diabetes isn’t theoretical anymore — it’s happening right now, cell by cell, gene by gene, and patient by patient.
Key References and Sources
Shapiro AMJ et al. N Engl J Med. 2023 — FDA approval of Lantidra (donislecel).
Vertex Pharmaceuticals press releases, 2023–2025 — VX-880 and VX-264 trial data.
ViaCyte / CRISPR Therapeutics updates on gene-edited hypoimmunogenic islets.
Herold KC et al. N Engl J Med. 2019 — Teplizumab delays T1D onset.
Haller MJ et al. Diabetes Care. 2024 — Low-dose IL-2 and regulatory T-cell therapies in T1D.