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Faculty Detail    
Name NABIHA YUSUF
 
Campus Address VH 566A
Phone 205-934-7432
E-mail nabiha@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Dermatology  Dermatology Assistant Professor
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Assistant Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Assistant Professor
Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Assistant Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Structural Biology 
Cancer Biology 
Cell, Molecular, & Developmental Biology 
Genetics and Genomic Sciences 
Immunology 
Microbiology 
Neuroscience 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Nabiha Yusuf, Assistant Professor in the Department of Dermatology, completed her postgraduate (MS) studies in Microbiology at the RD University, Jabalpur, India. Her doctoral work (PhD) in cardiac immunology was carried out at Aligarh Muslim University, Aligarh, India. There, she performed clinical studies to evaluate the role of circulating autoantibodies in dilated cardiomyopathy. She joined UAB in 2001 as a Postdoctoral fellow in the Department of Dermatology at UAB. Her project focussed on the role of T-cell subsets in cutaneous contact hypersensitivity responses and 7,12-dimethylbenz(a)anthracene (DMBA) induced skin cancer. Here, she also studied the role of T-cell subsets in photodynamic therapy of solid tumors. She continued her work and became an Instructor in 2005. In 2009, she was appointed as Assistant Professor in the same Department. She is currently pursuing her studies on the role of Toll like receptors in skin cancer.

Society Memberships
Organization Name Position Held Org Link
American Association for Cancer Research  Active Member  www.aacr.org 
Society of Investigative Dermatology  Active Member  www.sidnet.org 

Research/Clinical Interest
Title
Innate immune mechanisms in tumor development
Description
Our laboratory is involved in evaluating the effect of environmental influences such as chemical carcinogens and ultraviolet radiation on the skin immune system. The focus of our research is on the role of innate immunity in the development of skin carcinogenesis. Toll-like receptors (TLRs), one component of innate immunity, are intricately associated with a number of dermatologic conditions. We have found that the innate immune system mediates through Toll like receptor-4 (TLR4) signaling to activate the cell mediated adaptive immune response against chemically induced tumors. TLR4 signaling had a protective effect against 7,12-dimethylbenz(a)anthracene (DMBA) induced skin cancer in certain strains of mich which develop cell mediated immune response to this chemical carcinogen. We are currently in the process of evaluating the role of the innate immune system in ultraviolet B (UVB) radiation induced skin cancer. The mechanisms by which UVB radiation influences cell mediated immune responses have been the subject of extensive investigation. However, there is little information on the role of innate immunity in this process. Our recent experiments suggest that certain components of innate immunity, especially TLR4, may play an important role in photoimmunosuppression. Currently, we are investigating whether the resistance of TLR4 gene knockout mice to UVB-induced immunosuppression has implications for photocarcinogenesis. The ultimate goal of these studies will be to define the role of TLR4 in the development of immune suppression and tumor development that occurs following UV radiation. This may allow us to identify genetic loci that are involved in these processes and to develop immunopreventive and immunotherapeutic approaches toward them.

Selected Publications 
Publication PUBMEDID
Ahmad I, Simanyi E, Guroji P, Tamimi IA, delaRosa HJ, Nagar A, Nagar P, Katiyar SK, Elmets CA, Yusuf N. 2013. Toll-Like Receptor-4 deficiency enhances repair of ultraviolet radiation induced cutaneous DNA damage by nucleotide excision repair mechanism. J Invest Dermatol. 2013 Dec 10. doi: 10.1038/jid.2013.530.  24326454 
He D, Li H, Yusuf N, Elmets CA, Athar M, Katiyar SK, Xu H. 2012. IL-17 mediated inflammation promotes tumor growth and progression in the skin. PLos One 7:e32126.   22359662 
Naseemuddin M, Iqbal A, Nasti TH, Ghandhi JL, Kapadia AD, Yusuf N. 2011. Cell mediated immune responses through TLR4 prevents DMBA-induced mammary carcinogenesis in mice. Int J Cancer. 130:765-74.   21455984 
Lewis W, Simanyi E, Li H, Thompson CA, Nasti TH, Jaleel T, Xu H, Yusuf N. 2011. Regulation of ultraviolet radiation induced cutaneous photoimmunosuppression by Toll like receptor-4. Arch. Biochem. Biophys 508: 171-177.   21236239 
Nasti TH, Iqbal O, Geise JT, Katiyar SK, Yusuf N. 2011. Differential roles of T-cell subsets in regulation of ultraviolet radiation induced cutaneous photocarcinogenesis. Photochem Photobiol 87: 387-398.   21143237 
He D, Li H, Yusuf N, Elmets CA, Li J, Mountz J, Xu H. 2010. IL-17 promotes tumor development through the induction of tumor promoting microenvironments at tumor sites and myeloid derived suppressor cells. J Immunol. 184:2281-8.  20118280 
Yusuf N, Nasti TH, Huang CM, Huber BS, Jaleel T, Lin HY, Xu H, Elmets CA. 2009. Heat shock proteins HSP27 and HSP70 are present in the skin and are important mediators of allergic contact hypersensitivity. J Immunol., 182:675-83.  19109201 
Yusuf N, Nasti TH, Katiyar SK, Jacobs MK, Seibert MD, Ginsburg AC, Timares L, Xu H, Elmets CA. 2008. Antagonistic roles of CD4+ and CD8+ T-Cells in 7,12-dimethylbenz(a)anthracene cutaneous carcinogenesis. Cancer Res., 68 :3924-30   18483278 
Yusuf N, Nasti TH, Long JA, Naseemuddin M, Lucas AP, Elmets CA. 2008. Protective role of TLR4 during the initiation stage of cutaneous chemical carcinogenesis. Cancer Res., 68: 615-622.   18199559 

Keywords
toll like receptors, immune system, cancer, T-cells