òòò½Íø

Biography

Dr Melissa Ng attained her Bachelors in Science (Biomedical Science) from Imperial College London in 2012. She then moved to the University of California, San Francisco (UCSF), where she worked under Dr Trevor Burt for her Ph.D. uncovering the role of Helios driving the preferential differentiation of regulatory T cell differentiation in early life. In 2019, Melissa obtained her Ph.D. and returned to òòò½ÍøImmunology Network (SIgN) for her postdoctoral work under Dr Ng Lai Guan, where she studied how neutrophils undergo deterministic reprogramming in the tumor microenvironment, adopting a pro-angiogenic, phenotype that supports tumor growth.

In 2024, Melissa started her own research group after the award of the Career Development Fund (CDF) in 2020 and National Medical Research Council (NMRC) Young Investigator Research Grant (OF-YIRG) in 2024. Her current research ties together her broad expertise across both innate and adaptive arms of the immune system and will utilize cutting edge sequencing and in vitro/vivo functional assays to study the mechanisms of immune regulation, resolution and tolerance.  

Main Appointments

• Group Leader, òòò½ÍøImmunology Network (SIgN, A*STAR, Singapore)

Research Focus

Mechanisms of immune regulation, resolution and tolerance:

The immune system exists in a finely tuned balance between sterilizing immunity and tolerance, where activation of a highly inflammatory response is eventually resolved with a return to homeostasis to minimize collateral damage to the host. Consequently, failure to control inflammation and re-establish tolerance is central to the pathology of chronic diseases such as autoimmunity and chronic respiratory diseases. On the flip side, hijacking of immune resolution or tolerance mechanisms in cancer lead to increased tumor growth due to aberrant angiogenesis and immunosuppression. Understanding the mechanisms by which immune regulation, resolution and tolerance are enacted in homeostasis will be critical towards combating chronic diseases.

Research in the lab broadly follow three main themes:

(1)    Understanding the mechanisms driving tolerance and immune resolution at steady state

Tolerance of self, microbial and other innocuous antigens begin in early life. Regulatory T cells (Tregs) play a significant role maintaining tolerance, and the absence of FOXP3 expressing regulatory T cells lead to miscarriage, preterm births and autoimmunity. Circulating and tissue Treg numbers are highly elevated in early life, yet, yet output from the thymus is unchanged compared to adults. Understanding the spatial and temporal requirements for Treg conversion in the periphery in fetal/neonates will aid in modulation of Treg responses to enact tolerance to peripherally encountered antigens.

(2)    Breaking of tolerance and/or imperfect resolution in chronic inflammatory diseases

Bronchopulmonary dysplasia (BPD) is a severe lung disease of preterm infants, and remains the most common complication associated with prematurity. Systemic inflammation precedes the symptomatic onset of BPD, thus representing a therapeutic window of opportunity to divert the disease course. Currently, corticosteroids constitute the proven clinical modality to combat inflammation in BPD, but can result in neurological deficits and greater mortality in treated groups. As such, there is a critical need for immunomodulatory drugs that specifically target local lung inflammation without detrimental systemic side effects. Utilizing a 2-hit model of BPD, the failure and/or dysregulation of tolerance and resolution mechanisms can be tracked as the disease progresses.

(3)    Engineering tolerance and resolution

Specific modulation of the immune system to favor tolerance or disease resolution represents an attractive target in settings of chronic inflammatory disease, as current treatments focus on symptomatic relief or targeting ongoing inflammation without achieving cure. The lab aims to investigate methods of engineering immune cells with capabilities such as the enhanced secretion of pro-resolving soluble mediators, leveraging on their ability to migrate to the inflamed tissue site and kickstart the natural induction of tolerance or disease resolution. 

Lab Members

Publications

Publications_Melissa Ng (last updated on 27 January 2025)