Molecular mechanisms of CD8+ T cell-mediated delayed hypersensitivity: Implications for allergies, asthma, and autoimmunity

被引:104
作者
Kalish, RS [1 ]
Askenase, PW
机构
[1] SUNY Stony Brook, Hlth Sci Ctr, Dept Dermatol, Stony Brook, NY 11794 USA
[2] Yale Univ, Sch Med, New Haven, CT USA
关键词
T lymphocytes; CD8+; delayed hypersensitivity; allergic contact dermatitis; drug eruptions; asthma;
D O I
10.1016/S0091-6749(99)70489-6
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Delayed-type hypersensitivity (DTH) is defined as the recruitment of T cells into tissues to be activated by antigen-presenting cells to produce cytokines that mediate Local inflammation. CD8+ T cells are now known to mediate DTH responses in allergic contact dermatitis, drug eruptions, asthma, and autoimmune diseases. This inflammatory effector capability of CD8+ cytotoxic T cells was previously poorly recognized, but there is now considerable evidence that these diseases may be mediated by CD8+ DTH. The difference between CD8+ T cells and CD4+ T cells mediating DTH relates to the molecular mechanisms by which antigens are processed and presented to the T cells. Antigens external to the cell are phagocytosed and processed for presentation on MHC class II molecules (eg, HLA-DR) to CD4+ T cells. In contrast, internal cytoplasmic antigens are processed by the endogenous pathway for presentation on MHC class I molecules (eg, HLA-A, -B, and -C) to CD8+ T cells, External allergens can also enter the endogenous pathway to be presented to CD8+ T cells. These include many contact sensitizers, chemical and protein respiratory allergens, viral antigens, metabolic products of drugs, and autoantigens. The resulting CD8+ T-cell response explains the role of CD8+ T-cell DTH mechanisms in allergic contact dermatitis, asthma, drug eruptions, and autoimmune diseases.
引用
收藏
页码:192 / 199
页数:8
相关论文
共 101 条
[1]  
ANETT FC, 1984, SPONDYLOARTHROPATHIE, P297
[2]  
Baer H, 1986, Clin Dermatol, V4, P152, DOI 10.1016/0738-081X(86)90074-X
[3]   THE CTLS KISS OF DEATH [J].
BERKE, G .
CELL, 1995, 81 (01) :9-12
[4]   DIVERSITY OF ENDOGENOUS EPITOPES BOUND TO MHC CLASS-II MOLECULES LIMITED BY INVARIANT CHAIN [J].
BODMER, H ;
VIVILLE, S ;
BENOIST, C ;
MATHIS, D .
SCIENCE, 1994, 263 (5151) :1284-1286
[5]   Contact hypersensitivity in MHC class II-deficient mice depends on CD8 T lymphocytes primed by immunostimulating Langerhans cells [J].
Bouloc, A ;
Cavani, A ;
Katz, SI .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1998, 111 (01) :44-49
[6]   MAJOR HISTOCOMPATIBILITY COMPLEX CLASS I-RESTRICTED CD8(+) T-CELLS AND CLASS II-RESTRICTED CD4(+) T-CELLS, RESPECTIVELY, MEDIATE AND REGULATE CONTACT SENSITIVITY TO DINITROFLUOROBENZENE [J].
BOUR, H ;
PEYRON, E ;
GAUCHERAND, M ;
GARRIGUE, JL ;
DESVIGNES, C ;
KAISERLIAN, D ;
REVILLARD, JP ;
NICOLAS, JF .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1995, 25 (11) :3006-3010
[7]   ASSAY OF PROTEIN-QUINONE COUPLING INVOLVING COMPOUNDS STRUCTURALLY RELATED TO ACTIVE PRINCIPLE OF POISON IVY [J].
BYCK, JS ;
DAWSON, CR .
ANALYTICAL BIOCHEMISTRY, 1968, 25 (1-3) :123-&
[8]   Patients with allergic contact dermatitis to nickel and nonallergic individuals display different nickel-specific T cell responses.: Evidence for the presence of effector CD8+ and regulatory CD4+ T cells [J].
Cavani, A ;
Mei, D ;
Guerra, E ;
Corinti, S ;
Giani, M ;
Pirrotta, L ;
Puddu, P ;
Girolomoni, G .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1998, 111 (04) :621-628
[9]  
CHER DJ, 1987, J IMMUNOL, V138, P3688
[10]  
CLAESEN M, 1982, DRUG METAB DISPOS, V10, P667