RESEARCH
Biological mechanisms.
Reproducible measurement.
Skin is the body’s largest barrier, and most infections, injuries and environmental stresses meet it first. We study how barrier tissues sense damage, defend themselves and recover, and we build the reference materials that let such biology be measured the same way in every laboratory.
THEME 01
Skin biology and tissue repair
Skin heals most wounds within days. Yet the same repair programme can fail to start, as in chronic wounds, or refuse to stop, as in fibrosis and scarring. We want to understand the very first decision in that process: how a resting epidermis recognises that it has been injured, and how it switches into repair.
Part of the answer turns out to be mechanical. When a wound releases tension in the epidermis, the DNA methyltransferase DNMT3a moves into the nucleus of nearby differentiated keratinocytes and silences genes such as caspase-8, whose loss sets the repair programme in motion. Mechanical and epigenetic signals meet at that moment.
We are now following the same logic into the dermis. Using collagen contraction assays, ex vivo human skin and single-cell RNA sequencing, we ask how fibroblasts choose between orderly healing and fibrosis.
Key papers: PLOS Biology 2022 · Bio-protocol 2018 · Cell Communication & Adhesion 2013
THEME 02
Antimicrobial peptides and host defense
Skin makes its own antibiotics. Keratinocytes store and release antimicrobial peptides that kill bacteria and, as we have found, can also disable viruses. With antimicrobial resistance making common skin and wound infections harder to treat, strengthening this built-in defence is an appealing complement to conventional drugs.
We study how skin cells decide when, and how much, of these peptides to release. Psoriasin (S100A7) is secreted in two waves after contact with bacteria, and the second, sustained wave depends on the loss of caspase-8, the same change seen in inflammatory skin disease. The peptide LL37 breaks open the membrane of SARS-CoV-2, and niacinamide strengthens this effect. Most recently, we found that the fatty acid 12-hydroxystearic acid prompts keratinocytes to release peptides that block viral infection.
The questions ahead are which signals tune this release, and how broad the protection can be across bacteria and enveloped viruses.
Key papers: Cell Reports 2019 · Frontiers in Immunology 2023 · bioRxiv 2025 (preprint)
THEME 03
Virology and host–pathogen interactions
Dengue is now one of the fastest-spreading infections in the world, with more than 14 million cases reported in 2024, and India carries a large share of that burden. Lumpy skin disease, a poxvirus infection of cattle, has spread across the country since 2019. Progress against both depends on assays that measure infection and neutralisation reliably, and on antivirals that are affordable to develop.
We work with all four dengue virus serotypes, SARS-CoV-2 and lumpy skin disease virus in cell culture, using neutralisation and pseudotyped-virus assays with careful dose–response modelling. With collaborators, we test host-derived molecules and biologically synthesised nanomaterials for antiviral activity, and we work towards neutralisation measurements that can be compared across serotypes and laboratories.
Key papers: Frontiers in Immunology 2023 · bioRxiv 2025 (preprint)
THEME 04
Cellular health and circadian skin biology
Skin keeps time. Its cells run a circadian clock that shapes when the barrier repairs itself, when its lipids are made and how well it withstands ultraviolet light. Mitochondria, meanwhile, set how well those cells cope with stress. When either system falters, as it does with sun exposure and ageing, the barrier weakens, inflammation rises and pigmentation changes.
We study how mitochondrial stress in keratinocytes alters the signals they send to neighbouring cells, and how the epidermal clock controls the genes that build the skin’s lipid barrier. The work uses primary human keratinocytes and ex vivo human skin, imaging of mitochondrial networks and mitophagy, measurements of oxidative stress and energy status, and clock-gene time courses analysed with cosinor models.
THEME 05
Biological reference materials and measurement
A diagnostic test is only as good as the standard it is calibrated against. If two laboratories test the same sample and report different numbers, neither result can be fully trusted. World Health Organization reference reagents for dengue virus RNA exist, but they are scarce and imported.
Under the Indigenisation of Diagnostics (InDx) Program, a collaboration between the National Centre for Biological Sciences (NCBS) and the Centre for Cellular and Molecular Platforms (C-CAMP), we develop secondary reference reagents for all four dengue virus serotypes, traceable to the WHO reagents. The work covers production, unit assignment, vial-to-vial uniformity and stability, and a collaborative study in which four laboratories measured the reagents on their own instruments. The same approach has been applied to SARS-CoV-2.
Next, we aim to make these reagents easier to ship and store, and to extend the approach to other viruses that matter for human and animal health.
Research through collaboration
Our work is carried out with colleagues at the National Centre for Biological Sciences (NCBS), the Centre for Cellular and Molecular Platforms (C-CAMP), the Colin Jamora Lab at Shiv Nadar Institution of Eminence and other institutions. Students and researchers join through these host institutions, and their work is credited there.
Meet the people