The ‘Speak Your Science’ Seminar

Speaker 1: Krishna Ashokkumar(SRF) Guide: Dr. Vasudevan Seshadri and Late Dr. Mohan Wani Title: Mesenchymal Stem Cell-Derived Extracellular Vesicles for Bone Repair Abstract: The Mesenchymal stem cells (MSCs) are extensively studied due to their therapeutic importance as they possess immense regenerative and immunomodulatory potential. However, the therapeutic potential of MSC-based therapies remains a challenge due to various factors like short lifespan of cells as well as risk of pulmonary thromboembolism. Extracellular Vesicles (EVs) derived from MSCs form an important component of their secretome and mimic the therapeutic potential of the parent cell. However, a significant role of MSC derived EVs in alleviation of various bone related disorders like osteoarthritis, osteoporosis, has been extensively studied and reported, but their pathophysiology in relation to chronic diabetes remain unexplored. In our experiments, we observed a significant decline in bone microarchitectural parameters in streptozotocin induced Type 1 Diabetes Mellitus (T1DM) murine model. The lack of insulin in the body disrupts the anabolic tone of bone remodeling, ultimately leading to skeletal fragility. Therefore, we propose to utilize cell-free exosome preparations for designing a therapeutic strategy for diabetes induced systemic bone loss and evaluate its regenerative capacity in restoring the bone remodeling and homeostasis.
Speaker 2: Ahmad Habib(SRF) Guide: Dr. Girdhari Lal Title: Investigating the effect of CCR6 on innate lymphoid cells in gut inflammation and autoimmunity Abstract: Innate lymphoid cells (ILCs) are a newly uncovered family of innate immune cells that mirror the characteristics and functions of T cells. ILCs are tissue-inhabitant lymphocytes devoid of antigen-specific receptors and have innate effector functions such as cytokine production, which are crucial for the body’s rapid defense against infections, particularly at barrier sites. It has been discovered that ILCs are selectively accumulated and activated in patients with inflammatory diseases such as IBD, because of a change in the cytokine/chemokine balance. Various chemokine receptors aid in the ILCs homing to the site of inflammation and one such player is CCR6. Therefore, zeroing on CCR6-expressing ILCs, we are investigating the role of CCR6-expressing ILCs in regulating colitis.
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