Reduced production of both Th1 and Tc1 lymphocyte subsets in atopic dermatitis (AD)

Clinical and Experimental Immunology - Tập 115 Số 1 - Trang 1-5 - 2001
Antonietta Lonati1, Stefano Licenziati2, Angelo Donato Canaris2, Simona Fiorentini2, Giorgio Pasolini3, Marco Marcelli3, Stefania Seidenari4, Arnaldo Caruso2, G. De Panfilis3
1Department of Dermatology, Spedali Civili, Insitute of Virology and Microbiology, University of Brescia, Italy.
2Institute of Virology and Microbiology, University of Brescia, Brescia,
3Department of Dermatology, Spedali Civili,
4Department of Dermatology, University of Modena, Modena, Italy

Tóm tắt

SUMMARY

An imbalance of interferon-gamma (IFN-γ)-bearing CD4+ T (Th1) cells in the pathogenesis of AD is well recognized; however, a possible role in AD for CD8+ T cells secreting Th1-like cytokines (Tc1) has not been properly addressed. In this study, two- and three-colour FACS analysis allowed us to discriminate the Th1 from the Tc1 subset. AD patients had half the number of IFN-γ-producing circulating T cells (P < 0.005; 13.6 ± 1.9% (mean ± s.d.)) compared with normal donors (25.0 ± 2.4%). Specifically, both Th1 (4.8 ± 0.7%) and Tc1 (8.1 ± 1.1%) cells in AD were decreased compared with Th1 (8.8 ± 0.8%) and Tc1 (15.0 ± 1.5%) cells in controls. Moreover, at the mRNA level, the ratios of IFN-γ/IL-4 and IFN-γ/IL-10 were lower in cells from AD patients compared with controls. In conclusion, the decrease of IFN-γ-producing T lymphocytes in AD is due to a reduction in both Th1 and Tc1 IFN-γ-secreting cells; this may not only contribute to the over-production of IgE, but also explain the high incidence of cutaneous infections observed in AD patients.

Từ khóa


Tài liệu tham khảo

Mosmann TR, 1986, J Immunol, 136, 279, 10.4049/jimmunol.136.7.2348

Del Prete GF, 1991, J Clin Invest, 88, 346, 10.1172/JCI115300

10.1016/0167-5699(96)80606-2

10.1016/S0167-5699(97)80019-9

Ohmen JD, 1995, J Immunol, 154, 1956, 10.4049/jimmunol.154.4.1956

10.1111/1523-1747.ep12331164

10.1016/S0140-6736(94)90879-6

Wierenga EA, 1990, J Immunol, 144, 4651, 10.4049/jimmunol.144.12.4651

Reinhold U, 1991, Clin Exp Immunol, 86, 444, 10.1111/j.1365-2249.1991.tb02951.x

Kapsenberg ML, 1992, J Invest Dermatol, 82, 825

10.1046/j.1365-2133.1996.d01-1098.x

Reinhold U, 1990, Clin Exp Immunol, 79, 374, 10.1111/j.1365-2249.1990.tb08098.x

Wierenga EA, 1991, J Immunol, 147, 2942, 10.4049/jimmunol.147.9.2942

Van Der Heijden F, 1991, J Invest Dermatol, 97, 389, 10.1111/1523-1747.ep12480966

Jujo K, 1992, J Allergy Clin Immunol, 90, 323, 10.1016/S0091-6749(05)80010-7

Tang M, 1994, Clin Exp Immunol, 95, 66, 10.1111/j.1365-2249.1994.tb06016.x

Jung T, 1995, J Allergy Clin Immunol, 96, 515, 10.1016/S0091-6749(95)70296-2

Lester MR, 1995, J Immunol, 154, 6174, 10.4049/jimmunol.154.11.6174

Nakazawa M, 1997, J Allergy Clin Immunol, 99, 673, 10.1016/S0091-6749(97)70030-7

Nakagawa S, 1998, Exp Dermatol, 7, 112, 10.1111/j.1600-0625.1998.tb00310.x

Caruso A, 1995, J AIDS Human Retrovir, 10, 462

Hanifin JM, 1980, Acta Dermatol Venereol, 92, 44, 10.2340/00015555924447

23 DYM Leung, AR Rhodes, PS Geha, L Schneider, and J Ring . Atopic dermatitis. In: Fitzpatrick TB, Eisen AZ, Wolff Ket al., eds. Dermatology in general medicine. New York: McGraw-Hill, 1993 :1543, 64 .

Sanders B, 1991, Immunol Rev, 119, 65, 10.1111/j.1600-065X.1991.tb00578.x

10.1016/0022-1759(93)90158-4

Borthwich NJ, 1994, AIDS, 8, 431, 10.1097/00002030-199404000-00004

Graziosi C, 1994, Science, 265, 248, 10.1126/science.8023143

Yamamura M, 1992, J Immunol, 149, 1470, 10.4049/jimmunol.149.4.1470

10.1016/0167-5699(94)90152-X

Fong TAT, 1990, J Immunol, 144, 1744, 10.4049/jimmunol.144.5.1744

Croft M, 1994, J Exp Med, 180, 1715, 10.1084/jem.180.5.1715

Carter LL, 1995, J Immunol, 155, 1028, 10.4049/jimmunol.155.3.1028

Lacour M, 1993, Clin Rev Allergy, 11, 491

10.1016/1074-7613(95)90051-9

Cronin DC, 1995, J Immunol, 154, 3118, 10.4049/jimmunol.154.7.3118

Seder RA, 1995, J Exp Med, 181, 5, 10.1084/jem.181.1.5