Naqvi RA

About

My passion is cure Type1 Diabetes by transplantation of beta cells. Presently I am working to generate Neo-beta cells for imminent transplantation in Type 1 Diabetes patients with minimum immunosuppression. I have developed a protocol for the conversion of somatic cells into insulin producing cells within 14 days-which is completely unheard of so far. Maximum exploration of this protocol can be helpful in answering donor islet shortage issue associated with islet-transplantation in Type 1 diabetes patients. Before, that I was working on xenotransplantation of pig islets in pig to monkey xenotransplantation models and developed immune stealth pigs using CRISPR-Cas9 mediated knock in technology. These pigs had knock out of GGTA 1 enzyme (resposnible for having most incompatible glycan at the surface of pig cells surface) and various natural immue suppressor molecules to overcome innate and adaptive immune system of host.

miRNAs - small and stable RNA molecule , can be utilized as the biomarkers for various cellular process is also my one the interests. For the first time, I have figured out miR375 drived from pig islets - can be used as bimarker to predict the engraftment of pig islets transplanted in hepatic portal vein of monkey models. We have observed that if post-transplantation miR375 peak go down after 28 days of transplantatiaon upto 3-7 fold and then furhter decline can be treated as engraftment of pig islets. On contray if the peak would not go down after 28 -30 days, then islets would be constatnly dying and releasing this miR375.

Earleir I have studied, miRNAs in regulating various immune dysregualtions in leprosy patient. For the first time, we have shown that loss of miR181a function as an underlying mechanism for loss of T cell sensitive or mainteance of T cells anergy in leprosy patients. Furtehrmore, we have observed FoxP3 as a double edged sword, as it can behave as both transcription repressor and transcriptional activator by virtue of interatcting with histone deacetylase (HDAC7 and HDAC9) and histone acetyl transferease (HAT) in T regs derived from leprosy patients. Molecular cross-talk of FoxP3 with HDAC7/9 and HAT turned out to be crux of this mechanism. This study redefine the fact that FoxP3 is a strong transcriptinal repressor, as we found it circumstancial dependent. In T regs obtained from end stage leporsy patients (LL), FoxP3 also binds a the promoter region of miR155 - an essential element for the competitive fitness of CD4+CD25+ FoxxP3+ T regs. IN this pursuit, I have for the first time shown the presence of TCR (gamma delta )+ FoxP3+ cells as another dimension of immune suppression in leprosy patients progressing towards advance forte of disease (from BT/TT to BL/LL).

Employment

• University of Illinois Research Assistant Professor
  2020 - Present
• University of Illinois at Chicago Research Assistant Professor
  2020 - Present
• Indiana University Postdoctoral Researcher
  2018 - 2020
• University of Minnesota Postdoctoral Associate
  2013 - 2018
• All India Institute of Medical Sciences Postdoctoral Fellow
  2008 - 2013

Education

Education history is unavailable.

Projects & Funding

Projects & funding information is unavailable.

Publications

Publications are unavailable.