Immunobiology of Corneal Transplants

Immune Privilege and Retinal Transplantation

Effects of Ultraviolet-B on Contact Hypersensitivity

Current Research Projects:

Effects of Ultraviolet-B on Contact Hypersensitivity

The skin and the eye have alternative strategies to exploit immune protection against local pathogens. Whereas the eye arranges for immune protection that is selectively deficient in intense immunogenic inflammation, the skin selects immune mediators that are potent induces of inflammation. The immune response associated with the skin is modified upon exposure of cutaneous surface to ultraviolet-B radiation (the oncogenic component of sunlight), leading to tolerance and unresponsiveness. After UVB radiation, dermal antigen presenting cells take the place of epidermal Langerhans cells in delivering immunogenic/tolerogenic signals to the immune apparatus. Our experimental goals are to understand (a) the molecular mediators that modify cutaneous immunity following UVB radiation, (b) the phenotype of the dermal cells that promote hapten-specific tolerance, and (c) the genetic polymorphisms that render some individuals highly susceptible to the immune-damaging effects of sunlight. These studies have implications for the pathogenesis of sunlight-induced skin cancers, psoriasis, and allergic contact dermatitis.

Current Collaborator
Sharmila Masli, Ph.D.

Papers Published/In Press since January 1, 2002.

Kurimoto, I., Kitazawa, T., and Streilein, J.W. Studies of delayed systemic effects of ultraviolet B radiation on the induction of contact hypersensitivity. 2. Evidence that IL-10 from UVR-treated epidermis is the critical factor. Immunology 99:134 – 140, 2000.

Kurimoto, I., Kitazawa, T. and Streilein, J.W. Role of hapten dose in induction of tolerance through normal and ultraviolet-B exposed skin. J. Dermatological Science 24: 48 – 59, 2000.

Kitazawa, Toshiki, and Streilein, J.W. Studies of delayed systemic effects of ultraviolet B radiation on the induction of contact hypersensitivity. 3. Dendritic cells from secondary lymphoid organs are deficient in co-stimulatory signals that promote activation and differentiation of Th1 cells. Immunology 99: 296 – 304, 2000.
Xie, Yong, Li, Y., Zhang, Q., Stiller, M.J., Wang, C-L.A., and Streilein, J.W. Haptoglobin is a natural regulator of Langerhans cell function in the skin. J. Dermatologic Science 24: 25 – 37, 2000.

Kitazawa, T., and Streilein, J.W. Hapten-specific tolerance promoted by calcitonin gene-related peptide. J. Invest. Dermatol. 115: 942 – 948, 2000.

Alard, P., Kurimoto, I., Niizeki, H., and Streilein, J.W. Hapten-specific tolerance induced by acute, low dose ultraviolet B radiation of skin requires mast cell degranulation. Eur. J. Immun. 31: 1736 – 1746, 2001.

Bacci, S., Alard, P., and Streilein, J.W. Evidence that ultraviolet B radiation transiently inhibits emigration of Langerhans cells from exposed epidermis, thwarting contact hypersensitivity induction. Eur. J. Immunol. 31: 3588 – 3594, 2001.

Niizeki, H., Naruse, T., Hecker, K., Taylor, J. R., Kurimoto, I., Shimizu, T., Yamasaki, Y., Akiya, K., Tojo, T., Inoko, H., and Streilein, J.W. Polymorphisms in the TNF gene are associated with susceptibility to the effects of ultraviolet-B radiation on induction of contact hypersensitivity. Tissue Antigens 58: 369 – 378, 2001.