Summary
Researchers at the National Institute of Immunology, New Delhi, led by Soumen Basak, have shown in mice that the protein RelB is needed to produce IL-23-making dendritic cells in tiny immune outposts of the gut wall called solitary isolated lymphoid tissues.
In mice lacking RelB in these cells, the protective cell population nearly vanished. RelB does this by switching on another protein, RBP-J, which opens a separate signalling network. Earlier work from the same lab found RelB worsens chronic gut inflammation by suppressing regulatory T-cells in nearby lymph nodes.
The study, published in PNAS, is preclinical and its authors and outside experts caution that the findings must be extended before they apply to patients.
WHY IT MATTERS FOR UPSC & STATE PCS
A study by the National Institute of Immunology, New Delhi, published in PNAS and reported by The Hindu on 19 October 2026, shows that RelB plays opposite roles in gut immunity depending on location - a finding relevant to designing safer, targeted therapies for inflammatory bowel disease.
Standard News
The Same Protein Builds the Gut's Alarm System and Disarms Its Peacekeepers
Here's what's actually happening. The gut has to fight harmful microbes without attacking the trillions of harmless ones living there. Too weak a response lets infections settle; too strong a response turns the immune system against the gut itself, as in Crohn's disease and other forms of inflammatory bowel disease (IBD).
The National Institute of Immunology study, published in PNAS, traces part of this balance to one protein: RelB.
The mechanism, step by step Deep in the intestinal wall sit small immune outposts called solitary isolated lymphoid tissues (SILTs).
Inside them are dendritic cells, the immune system's messengers, which detect threats and alert other immune cells. Some of these act as sentinels, releasing IL-23, a signalling molecule that triggers protective inflammation.
The NII team, led by Soumen Basak, bred mice lacking RelB in these cells. The IL-23-producing sentinel population almost vanished. Earlier thinking was that RelB merely helped existing cells make IL-23. The team found instead that losing RelB mainly reduced the number of these cells.
The route runs through a second protein. RelB switches on RBP-J, which opens a separate signalling network. Only when both act do immature cells become IL-23-producing sentinels. Two systems long thought to work independently turn out to work together.
Why one protein can play opposite roles In nearby lymph nodes, the same RelB suppresses regulatory T-cells
- the immune system's peacekeepers. Earlier work from Basak's lab showed this worsens chronic gut inflammation. UCLA immunologist Alexander Hoffmann, as reported, offered an explanation. RelB is a weaker activator than its relative RelA. Think of two keys for a set of locks:
- where both keys fit, the weaker RelB key occupies the lock and stops the stronger one turning it - so RelB acts like a brake; - where only RelB fits, its weak turn is still enough to open the door - so it acts as an activator, including for the gene behind gut defences. The analogy has limits: genes are controlled by many proteins working together, not one key at a time. But it captures why location decides RelB's effect.
What this means for treatment Drugs that block IL-23 are already frontline IBD treatments.
The study suggests why such blunt blockade carries risk: the same signals that drive harmful inflammation also build the gut's defence against bacteria. Future biologics may need to be tissue-specific
- calming inflammation in one place without dismantling protection in another. This is still mouse research. Saurabh Mehandru of Mount Sinai cautioned, as reported, that the findings must be extended before they guide patient care. The team also cannot yet say whether RelB builds these cells or only keeps them alive.
Where
India stands India has an estimated 1.4-1.5 million people with IBD, among the largest burdens in the world and cases are rising. NII, an autonomous institute under the Department of Biotechnology since 1981, is producing basic science that targeted therapies will depend on.
Quick Facts
Key numbers & takeaways — revise these first
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The study was conducted at the National Institute of Immunology (NII), New Delhi and published in the Proceedings of the National Academy of Sciences (PNAS).
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It was led by immunologist Soumen Basak.
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The research used mice engineered to lack RelB in specific gut immune cells.
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IL-23 is a signalling molecule that triggers protective inflammation at barrier surfaces such as the gut.
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Without RelB, IL-23-producing dendritic cells in solitary isolated lymphoid tissues nearly disappeared.
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RelB acts by switching on the protein RBP-J, which unlocks a separate signalling network.
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Drugs blocking IL-23 are frontline treatments for inflammatory bowel disease.
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India has an estimated 1.4 to 1.5 million people with inflammatory bowel disease.
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NII was founded in 1981 as an autonomous institute under the Department of Biotechnology.
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Crohn's disease and ulcerative colitis are the two main forms of inflammatory bowel disease.
Connect the dots for your UPSC preparation.
Standard news covers the event. Log in to read our comprehensive analysis and uncover the hidden constitutional, structural, and ethical dimensions of this topic:
A step-by-step map of the RelB to RBP-J to IL-23 relay and why finding that two signalling systems cooperate is the study's real advance.
The two-keys explanation for why RelB protects in one tissue and inflames in another and where that analogy stops working.
Why blunt IL-23 or RelB blockade could weaken antibacterial defence and what tissue-specific targeting would require.
India's IBD burden, the role of DBT and NII and the hurdles in moving from mouse models to Indian patients.
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