Biography
Thanks to the sacrifices made by my parents, I could afford to have excellent higher education after being selected by the best institutions in India at that time. I received B.Sc. at Presidency College, Kolkata (Calcutta), India, which had exceptional alumni, such as, Satyendra Nath Bose (Bose-Einstein statistics); Swami Vivekananda; Rabindranath Tagore; Netaji Subhas Chandra Bose; 1st President of India (Rajendra Prasad) and Noble Laureates (Rabindranath Tagore in Literature; Amartya Sen in Economics, 1998; Abhijit Banerjee in Economics, 2019).
Next for my MD, I entered Medical College and Hospital, Kolkata, India, where Sir Ronald Ross worked out the lifecycle of Malarial Parasite (Nobel Prize in physiology and Medicine 1902); Upendranath Brahmachari synthesized urea stibamine (carbostibamide) in 1922 for treating Visceral Leishmaniasis (VL in Kala-azar) caused by Leishmania Donovani spread by sandfly bites.
Relevant to me in Medical School, I was the Class Assistant to my teacher Prof. Sambhu Nath De (S.N. De), who discovered Cholera Toxin and developed the basis of effective treatment of Cholera; using his rabbit ileal loop (RIL) method in 1953. In the words of Nobel Laureate Prof. Joshua Lederberg, who nominated S.N. De twice for Nobel Prize, “De’s clinical observations led him to the bold thought that dehydration was a sufficient cause of pathology of cholera, that the cholera toxin can kill ‘merely’ by stimulating the secretion of water into the bowel. Thus, the oral rehydration therapy (ORT) for replenishing the massive fluid loss in cholera patients, that has saved innumerable lives, should be considered as a direct outcome of De’s discovery of cholera toxin. His findings on exotoxins set the stage for the modern views of diseases caused by toxin producing bacteria, helped in the purification of cholera and heat-labile (LT) enterotoxins produced by V. cholerae and E. coli, respectively, and in the development of series of cholera and enterotoxigenic E. coli (in short ETEC strains) vaccines. The rapid development of studies in the first 5 years after the findings of enterotoxigenic E. coli (ETEC) was published by Prof. De, include the recognition that both heat-labile and heat-stable enterotoxins (LT and ST) were separate enterotoxin; and the discovery of pili (fimbria) as a critically important virulence factor for ETEC, in causing diarrhea of travelers”.
While completing my medical training internship in Calcutta medical college, my goal was to do disease relevant research based on Basic Immunologic mechanism of disease.
The best institutions to do such research were in USA. At that time (1968) there was a shortage of doctors in the US with the ongoing Vietnam War, especially in the city hospitals. So, I was hired by Mount Sinai’s City Hospital center Elmhurst in New York for internship, and then for residency at Cook County hospital, Chicago. Both hospitals admitted very sick patients, so we were “on call” every day. I had also signed up for the Draft. Interestingly, doctors stationed in Vietnam frequently came for Trauma Surgical training at Cook County hospital, which had close to 2000 beds at that time (1969).
After Residency, I completed a Fellowship in Hematology, and my mentors recommended me to Dr. Robert Schwartz for Research Fellowship at New England Medical Center, Tufts Medical School in Boston. Dr. Schwartz was also known as “Immunosuppression Schwartz”, since immunosuppressive drugs like Immuran, Cytoxan and such that are being used today for transplants and autoimmune diseases like lupus nephritis, were developed from his discoveries. I wanted to do research on Lupus, a systemic autoimmune disease and with its diverse immunological abnormalities was an excellent window to the immune system. At that time, most prominent lupus researchers with large grants were in pursuit of the “Lupus virus”. Especially endogenous retroviruses whose genomes had integrated into the host genome eons ago, were thought to be the culprits. I was assigned to work related to this dogma. However, I thought the evidence was not sufficient for a cause and effect relationship. Using Lupus prone mouse models that had genes determining expression of retroviruses, I found that those genes could be segregated from development of SLE (S.K. Datta, and R.S. Schwartz, Genetics of expression of xenotropic virus and autoimmunity in NZB mice. Nature. 263 (1976) 412-415. S.K. Datta, N. Manny, C. Andrzejewski, J. Andre-Schwartz, and R.S. Schwartz, Genetic studies of autoimmunity and retrovirus expression in crosses of New Zealand Black mice. I. xenotropic virus. J. Exp. Med. 147 (1978) 854-871). Thus, we showed that the endogenous retrovirus was another target autoantigen, but not the cause of autoimmunity. These studies contributed to a change in the emphasis in lupus research in the early 70’s, from the pursuit of a viral etiology to elucidating basic defects inherent in the lupus immune system that responds abnormally to autoantigens. My laboratory then showed that an endogenous self-antigen, namely nucleosomes from apoptotic cells, linked self-reactive lupus T helper (Th) and B cell with cognate interactions leading to the production of class-switched nephritogenic anti-dsDNA autoantibodies. Those initial findings led us to develop autoantigen-specific therapy of lupus. Based on these advances, I received grants from NIH to open my own laboratory as a principal investigator (1974, 1976) and then MERIT awards from NIH for further studies.
In 1993, I was selected for the Solovy Arthritis Research Society Endowed Chair at Northwestern University (NU), which I accepted; and NIH and Tufts University allowed me to move my grants to NU.
Most recently, I have completed an e-book: Generating and Sustaining Stable Autoantigen-specific CD4 and CD8 Regulatory T Cells in Lupus | Frontiers Research Topic (frontiersin.org). The book focuses on ways to enhance the body’s endogenous regulatory mechanisms, namely by generating specialized regulatory T cells that are targeted to suppress inflammatory autoreactive cells responsible for causing autoimmune disease, like lupus.