Immunology Today, voL 7, No. 12, 1986
-Ietters Lockwood, D.H. (1970) Ann. N. Y. Acad. Sci. 171,882498
14 Tarter, T.H. and Alexander, N.J. (1984) Am. J. Reprod. Immunol. 6, 28-32
Interactions between epidermal cells and lymphocytes in psoriasis Sir, H. Valdimarsson and his colleagues should be complimented for pointing out the significance of altered epidermal cell-lymphocyte interaction in psoriasis (ImmunoL Today, 1986, 7, 256-259). They develop the concept that psoriatic lesions are initiated by the accumulation of a putatively abnormal antigen in the dermis, presented on Langerhans' cells and propagated by the response of specific helper T (Th) cells crossing the dermal--epidermal junction. The end product of that reaction is the increased presence of HLA-DR + Th and Langerhans' cells in the epidermis. As lymphokines induce epidermal cell growth I, it seems conceivable that activated Th cells may initiate the abnormal epidermal cell proliferation that is
358
15 Richards, J.M., Bedford, J.M. and Witkin, S.S. (1984) Science 224, 390--392 16 Thomas, I.K. and McLean, J.M. (1984) Am. J. Reprod. ImmunoL 6, 185-189
17 Sachiko, K., Ryuji, U. and Hayaishi, O. (1986) Proc. Natl Acad. Sci. USA 83, 2682-2683 18 Hurtenbach, U. and Shearer, G.M. (1982)J. Exp. Med. 155, 1719-1729
characteristic in psoriasis. Studying the stimulation of enriched T cells by autologous, isolated epidermal cells (the autologous mixed epidermal cell-lymphocyte reaction, AMECLR), we found that the AMECLR in healthy controls (n=9) resembled that in psoriatic patients when the epidermal cells were isolated from uninvolved skin. However, in 10 psoriatic patients epidermal cells from the sites of lesions induced a significantly higher T cell proliferation in the AMECLR (p
-Ietters Lockwood, D.H. (1970) Ann. N. Y. Acad. Sci. 171,882498
14 Tarter, T.H. and Alexander, N.J. (1984) Am. J. Reprod. Immunol. 6, 28-32
Interactions between epidermal cells and lymphocytes in psoriasis Sir, H. Valdimarsson and his colleagues should be complimented for pointing out the significance of altered epidermal cell-lymphocyte interaction in psoriasis (ImmunoL Today, 1986, 7, 256-259). They develop the concept that psoriatic lesions are initiated by the accumulation of a putatively abnormal antigen in the dermis, presented on Langerhans' cells and propagated by the response of specific helper T (Th) cells crossing the dermal--epidermal junction. The end product of that reaction is the increased presence of HLA-DR + Th and Langerhans' cells in the epidermis. As lymphokines induce epidermal cell growth I, it seems conceivable that activated Th cells may initiate the abnormal epidermal cell proliferation that is
358
15 Richards, J.M., Bedford, J.M. and Witkin, S.S. (1984) Science 224, 390--392 16 Thomas, I.K. and McLean, J.M. (1984) Am. J. Reprod. ImmunoL 6, 185-189
17 Sachiko, K., Ryuji, U. and Hayaishi, O. (1986) Proc. Natl Acad. Sci. USA 83, 2682-2683 18 Hurtenbach, U. and Shearer, G.M. (1982)J. Exp. Med. 155, 1719-1729
characteristic in psoriasis. Studying the stimulation of enriched T cells by autologous, isolated epidermal cells (the autologous mixed epidermal cell-lymphocyte reaction, AMECLR), we found that the AMECLR in healthy controls (n=9) resembled that in psoriatic patients when the epidermal cells were isolated from uninvolved skin. However, in 10 psoriatic patients epidermal cells from the sites of lesions induced a significantly higher T cell proliferation in the AMECLR (p
