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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
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 
Sharma SD, Meeran SM, Katiyar N, Tisdale B, Yusuf N, Xu H, Elmets CA, Katiyar SK. IL-12-deficiency suppresses 12-O-tetradecanoylphorbol-13-acetate-induced skin tumor development in 7, 12-dimethylbenz(a)anthracene-initiated mouse skin through inhibition of inflammation. Carcinogenesis. 2009 Sep 16. [Epub ahead of print]  19759192 
Yusuf N, Nasti TH, Meleth S, Elmets CA. 2009. Resveratrol enhances cell-mediated immune response to DMBA through TLR4 and prevents DMBA induced cutaneous carcinogenesis. Mol. Carcinog., 48:713-23.  19142898 
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, Katiyar SK, Elmets CA. 2008. The Immunosuppressive Effects of Phthalocyanine Photodynamic Therapy in Mice Are Mediated by CD4+ and CD8+ T Cells and Can Be Adoptively Transferred to Naive Recipients. Photochem. Photobiol., 84: 366-370.  18208456 
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 
Elmets CA, Yusuf N, Hamza S, Iranikhah N, Smith J, Volk AL, Skelton H, Smith K. 2004. Topical application of Dimethylbenz(a)anthracene results in the generation of multiple melanocytic nevi in C3H/HeN mice. Toxicol Appl Pharmacol.,195:355-60.   15020198 
Huang, CM, Foster KW, DeSilva T, Zhang J, Shi Z, Yusuf N, Van Kampen, KR, Elmets CA and Tang DC. 2003. Comparative Proteomic profiling of Murine skin. J. Invest. Dermatol.,121:51-64.
 
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Keywords
toll like receptors, immune system, cancer, T-cells