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Faculty Detail    
Name RAJATAVA BASU
  
Campus Address BBRB 730A Zip 2170
Phone  (205) 934-8301
E-mail  rajatavabasu@uabmc.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Pathology   Molecular & Cellular Pathology Assistant Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Assistant Professor

Graduate Biomedical Sciences Affiliations
Immunology 

Biographical Sketch 
Rajatava Basu received his doctoral training both in India and Germany working at Indian Institute of Chemical Biology, India and Humboldt University, Berlin, Germany. During his Ph.D., he characterized an immunodominant epitope of antigen by proteomic analysis to develop an effective DNA vaccination strategy against visceral leishmanisis. In 2009 he joined laboratory of Prof. Casey Weaver at UAB for for his post-doctoral studies on area of cellular and molecular mechanisms controlling T cell-mediated immune regulation during autoimmune inflammation with a specific focus on understanding pathogen-mediated dysregulated host immune response in intestinal bowel disease. He joined UAB as tenure-earning Assistant Professor in Oct 2017.

Society Memberships
Organization Name Position Held Org Link
American Association of Immunologists   Member  http://www.aai.org/  
Crohn's & Colitis Foundation of America  Member  http://www.crohnscolitisfoundation.org 
 



Research/Clinical Interest
Title
Cellular and molecular mechanisms controlling CD4 T cell-mediated immune regulation during inflammation.
Description
1. Understanding the role of orphan- and non-orphan nuclear receptors in CD4+T cell development in autoimmune disease and cancer. Nuclear receptors are orphaned or ligand-dependent transcription factors that have important roles in several biological processes, including cell proliferation, differentiation and cellular homeostasis. Nuclear receptors provide a unique resource for uncovering novel regulatory systems that impact human health and also provide drug targets (agonist and antagonists) for a variety of human diseases including autoimmune diseases, cancers, neurodegenerative diseases, skin disorders and diabetes. Study on nuclear receptors represents a tremendous opportunity in understanding and treating several human diseases. 2. Intrinsic signaling pathways modulating CD4+ T cell commitment along effector/regulatory axis in the intestinal immune response. Plasticity can be defined as the ability of a single CD4+ T cell to take on characteristics of many CD4+T cell subsets simultaneously or at different times during the course of its life cycle. This can occur by transitions induced during a metastable T cell state or reprogramming between subsets. Among all the discovered CD4 T helper cell subsets, Th17 cells exhibit the highest degree of plasticity. Th17 cells are unstable as a phenotype (‘plastic’) and can easily trans-differentiate from or into other T helper cell phenotypes like T helper 1 (Th1), T helper 22 (Th22) and inducible regulatory T cells (iTreg) cells. Therefore, differentiation of Th17 cells is a highly dynamic process (‘plastic’) with overlapping developmental axes with iTreg, Th22 and Th1 cells. Accordingly, intermediary stages of Th17 cells are found in various tissues, which co-express lineage-specific transcription factor(s) or cytokine(s) of developmentally related CD4 T cell subsets. Currently, Th17 plasticity remains an unresolved concern in the field of clinical research as targeting Th17 cells to cure immune-mediated disease might also target its related subsets. Stemming from a series of observations, the research would broadly focuses on dynamic regulation of mucosal immune response of the intestine by investigating the cellular, molecular and epigenetic characteristics of Th17 cells that tie its developmental axis to iTreg, Th22 and Th1 cells in autoimmune disease and cancer models. POSITIONS AVAILABLE FOR GRADUATE STUDENTS. GRAD STUDENTS ARE WELCOME TO APPLY.

Selected Publications 
Publication PUBMEDID
SELECTED PUBLICATIONS
1. Mickael ME, Bhaumik S, Basu R. 2020. Retinoid-Related Orphan Receptor RORγt in CD4 + T-Cell-Mediated Intestinal Homeostasis and Inflammation. Am J Pathol. 2020 Oct;190(10):1984-1999. doi: 10.1016/j.ajpath.2020.07.010. Epub 2020 Jul 29. PMID: 32735890.

2. Basu R* & Bhaumik. S. 2017. Cellular and Molecular Dynamics of Th17 Differentiation and its Developmental Plasticity in the Intestinal Immune Response. Front. Immunol. 2017 Mar 31;8:254

3. Basu R, Whitley SK, Bhaumik S, Zindl CL, Schoeb TR, Benveniste EN, Pear WS, Hatton RD, Weaver CT. 2015. IL-1 signaling modulates activation of STAT transcription factors to antagonize retinoic acid signaling and control the TH17 cell-iTreg cell balance. Nat Immunol. March;16(3):286-95.

4. Basu R*, Hatton RD, Weaver CT. The Th17 family: flexibility follows function. 2013. Immunol Rev. Mar; 252(1):89-103. (*Corresponding author)

5. Basu R, O'Quinn DB, Silberger DJ, Schoeb TR, Fouser L, Ouyang W, Hatton RD, Weaver CT. 2012. Th22 cells are an important source of IL-22 for host protection against enteropathogenic bacteria. Immunity. 2012 Dec 14;37(6):1061-75.

6. Basu R, Roy S, Walden P. 2007. HLA class I-restricted T cell epitopes of the kinetoplastid membrane protein-11 presented by Leishmania donovani-infected human macrophages. J Infect Dis. 195(9):1373-80.

7. Basu R, Bhaumik S, Basu JM, Naskar K, De T, Roy S. 2005. Kinetoplastid membrane protein-11 DNA vaccination induces complete protection against both pentavalent antimonial-sensitive and -resistant strains of Leishmania donovani that correlates with inducible nitric oxide synthase activity and IL-4 generation: evidence for mixed Th1- and Th2-like responses in visceral leishmaniasis. J Immunol.174(11):7160- 71.
 		  
 

Keywords
CD4+ T cells; T Helper Cells; Retinoic acid receptor-related orphan receptor gamma t (RORgt); Aryl Hydrocarbon Receptor (AhR)