Contribution of CD4⁺ and CD8⁺ T-cells in contact hypersensitivity and allergic contact dermatitis

References

• Saint-Mezard P, Rosieres A, Krasteva M et al. Allergic contact dermatitis. Eur. J. Dermatol. 14(5), 284–295 (2004).
   PubMed Web of Science ®Google Scholar
• Blauvelt A, Hwang ST, Udey MC. Allergic and immunologic diseases of the skin. J. Allergy Clin. Immunol. 111(2 Suppl.), S560–S570 (2003).
   PubMed Web of Science ®Google Scholar
• Belsito DV. The diagnostic evaluation, treatment, and prevention of allergic contact dermatitis in the new millennium. J. Allergy Clin. Immunol. 105(3), 409–420 (2000).
   PubMed Web of Science ®Google Scholar
• Lepoittevin JP, Leblond I. Hapten-peptide T-cell receptor interactions: molecular basis for the recognition of haptens by T-lymphocytes. Eur. J. Dermatol. 7, 151–154 (1997).
   Web of Science ®Google Scholar
• Krasteva M, Kehren J, Ducluzeau MT et al. Contact dermatitis I. Pathophysiology of contact sensitivity. Eur. J. Dermatol. 9(1), 65–77 (1999).
   PubMed Web of Science ®Google Scholar
• Cavani A, Albanesi C, Traidl C, Sebastiani S, Girolomoni G. Effector and regulatory T-cells in allergic contact dermatitis. Trends Immunol. 22(3), 118–120 (2001).
   PubMed Web of Science ®Google Scholar
• Gorbachev AV, Fairchild RL. Regulatory role of CD4+ T-cells during the development of contact hypersensitivity responses. Immunol. Res. 24(1), 69–77 (2001).
   PubMedGoogle Scholar
• Watanabe H, Unger M, Tuvel B, Wang B, Sauder DN. Contact hypersensitivity: the mechanism of immune responses and T-cell balance. J. Interferon Cytokine Res. 22(4), 407–412 (2002).
   PubMed Web of Science ®Google Scholar
• Girolomoni G, Sebastiani S, Albanesi C, Cavani A. T-cell subpopulations in the development of atopic and contact allergy. Curr. Opin. Immunol. 13(6), 733–737 (2001).
   PubMed Web of Science ®Google Scholar
• Kalish RS, Askenase PW. Molecular mechanisms of CD8+ T-cell-mediated delayed hypersensitivity: implications for allergies, asthma, and autoimmunity. J. Allergy Clin. Immunol. 103(2 Pt 1), 192–199 (1999).
   PubMed Web of Science ®Google Scholar
• Dupuis GB. Nature of hapten–protein interactions. In: Chemically Reactive Function in Haptens and Proteins, in Allergic Contact Dermatitis to Simple Chemicals. A Molecular Approach. Calnan CD, Maibach HI (Eds), Marcel Dekker, Inc., NY, USA (1982).
   Google Scholar
• Berard F, Marty JP, Nicolas JF. Allergen penetration through the skin. Eur. J. Dermatol. 13(4), 324–330 (2003).
   PubMed Web of Science ®Google Scholar
• Dupuis GB. Studies on poison ivy. In vitro lymphocyte transformation by urushiol–protein conjugates. Br. J. Dermatol. 101(6), 617–624 (1979).
   PubMedGoogle Scholar
• Saloga J, Knop J, Kolde G. Ultrastructural cytochemical visualization of chromium in the skin of sensitized guinea-pigs. Arch. Dermatol. Res. 280(4), 214–219 (1988).
   PubMed Web of Science ®Google Scholar
• Anderson C, Hehr A, Robbins R et al. Metabolic requirements for induction of contact hypersensitivity to immunotoxic polyaromatic hydrocarbons. J. Immunol. 155(7), 3530–3537 (1995).
   PubMed Web of Science ®Google Scholar
• Martin S, Ortmann B, Pflugfelder U, Birsner U, Weltzien HU. Role of hapten-anchoring peptides in defining hapten-epitopes for MHC-restricted cytotoxic T-cells. Cross-reactive TNP-determinants on different peptides. J. Immunol. 149(8), 2569–2575 (1992).
   PubMed Web of Science ®Google Scholar
• Buckley DA, Rycroft RJ, White IR, McFadden JP. Fragrance as an occupational allergen. Occup. Med. 52(1), 13–16 (2002).
   Google Scholar
• Cumberbatch M, Dearman RJ, Griffiths CE, Kimber I. Epidermal Langerhans cell migration and sensitisation to chemical allergens. APMIS 111(7–8), 797–804 (2003).
   PubMed Web of Science ®Google Scholar
• Saint-Mezard P, Krasteva M, Chavagnac C et al. Afferent and efferent phases of allergic contact dermatitis (ACD) can be induced after a single skin contact with haptens: evidence using a mouse model of primary ACD. J. Invest. Dermatol. 120(4), 641–647 (2003).
   PubMedGoogle Scholar
• Sunday ME, Dorf ME. Hapten-specific T-cell response to 4-hydroxy-3-nitrophenyl acetyl. X. Characterization of distinct T-cell subsets mediating cutaneous sensitivity responses. J. Immunol. 127(2), 766–768 (1981).
   PubMedGoogle Scholar
• Gocinski BL, Tigelaar RE. Roles of CD4+ and CD8+ T-cells in murine contact sensitivity revealed by in vivo monoclonal antibody depletion. J. Immunol. 144(11), 4121–4128 (1990).
   PubMed Web of Science ®Google Scholar
• Bour H, Peyron E, Gaucherand M. Major histocompatibility complex class I-restricted CD8+ T-cells and class II-restricted CD4+ T-cells, respectively, mediate and regulate contact sensitivity to dinitrofluorobenzene. Eur. J. Immunol. 25(11), 3006–3010 (1995).
   PubMed Web of Science ®Google Scholar
• Cosgrove D, Gray D, Dierich A et al. Mice lacking MHC class II molecules. Cell 66(5), 1051–1066 (1991).
   PubMedGoogle Scholar
• Chan SH, Cosgrove D, Waltzinger C, Benoist C, Mathis D. Another view of the selective model of thymocyte selection. Cell 73(2), 225–236 (1993).
   PubMed Web of Science ®Google Scholar
• Bouloc A, Cavani A, Katz SI. Contact hypersensitivity in MHC class II-deficient mice depends on CD8 T-lymphocytes primed by immunostimulating Langerhans cells. J. Invest. Dermatol. 111(1), 44–49 (1998).
   PubMedGoogle Scholar
• Krasteva M, Kehren J, Horand F et al. Dual role of dendritic cells in the induction and downregulation of antigen-specific cutaneous inflammation. J. Immunol. 160(3), 1181–1190 (1998).
   PubMedGoogle Scholar
• Akiba H, Kehren J, Ducluzeau MT et al. Skin inflammation during contact hypersensitivity is mediated by early recruitment of CD8+ T cytotoxic 1 cells inducing keratinocyte apoptosis. J. Immunol. 168(6), 3079–3087 (2002).
   PubMed Web of Science ®Google Scholar
• Xu H, DiIulio NA, Fairchild RL. T-cell populations primed by hapten sensitization in contact sensitivity are distinguished by polarized patterns of cytokine production: interferon γ-producing (Tc1) effector CD8+ T-cells and interleukin (IL) 4/IL-10-producing (Th2) negative regulatory CD4+ T-cells. J. Exp. Med. 183(3), 1001–1012 (1996).
   PubMed Web of Science ®Google Scholar
• Kolesaric A, Stingl G, Elbe-Burger A. MHC class I+/II- dendritic cells induce hapten-specific immune responses in vitro and in vivo. J. Invest. Dermatol. 109(4), 580–585 (1997).
   PubMedGoogle Scholar
• Martin SF, Dudda JC, Delattre V et al. Fas-mediated inhibition of CD4+ T-cell priming results in dominance of Type 1 CD8+ T-cells in the immune response to the contact sensitizer trinitrophenyl. J. Immunol. 173(5), 3178–3185 (2004).
   PubMedGoogle Scholar
• Fehr BS, Takashima A, Matsue H, Gerometta JS, Bergstresser PR, Cruz PD Jr. Contact sensitization induces proliferation of heterogeneous populations of hapten-specific T-cells. Exp. Dermatol. 3(4), 189–197 (1994).
   PubMedGoogle Scholar
• Kehren J, Desvignes C, Krasteva M et al. Cytotoxicity is mandatory for CD8+ T-cell-mediated contact hypersensitivity. J. Exp. Med. 189(5), 779–786 (1999).
   PubMed Web of Science ®Google Scholar
• Martin S, Lappin MB, Kohler J et al. Peptide immunization indicates that CD8+ T-cells are the dominant effector cells in trinitrophenyl-specific contact hypersensitivity. J. Invest. Dermatol. 115(2), 260–266 (2000).
   PubMed Web of Science ®Google Scholar
• Gorbachev AV, Heeger PS, Fairchild RL. CD4+ and CD8+ T-cell priming for contact hypersensitivity occurs independently of CD40-CD154 interactions. J. Immunol. 166(4), 2323–2332 (2001).
   PubMedGoogle Scholar
• Buller RM, Holmes KL, Hugin A, Frederickson TN , Morse HC III. Induction of cytotoxic T-cell responses in vivo in the absence of CD4 helper cells. Nature 328(6125), 77–79 (1987).
   PubMed Web of Science ®Google Scholar
• Rahemtulla A, Fung-Leung WP, Schilham MW et al. Normal development and function of CD8+ cells but markedly decreased helper cell activity in mice lacking CD4. Nature 353(6340), 180–184 (1991).
   PubMed Web of Science ®Google Scholar
• Wang B, Norbury CC, Greenwood R, Bennink JR, Yewdell JW, Frelinger JA. Multiple paths for activation of naive CD8+ T-cells: CD4-independent help. J. Immunol. 167(3), 1283–1289 (2001).
   PubMed Web of Science ®Google Scholar
• Mintern JD, Davey GM, Belz GT, Carbone FR, Heath WR. Cutting edge: precursor frequency affects the helper dependence of cytotoxic T-cells. J. Immunol. 168(3), 977–980 (2002).
   PubMedGoogle Scholar
• Schuurhuis DH, Laban S, Toes RE et al. Immature dendritic cells acquire CD8+ cytotoxic T-lymphocyte priming capacity upon activation by T-helper cell-independent or -dependent stimuli. J. Exp. Med. 192(1), 145–150 (2000).
   PubMed Web of Science ®Google Scholar
• Berke G. The CTL’s kiss of death. Cell 81(1), 9–12 (1995).
   PubMed Web of Science ®Google Scholar
• Corazza N, Muller S, Brunner T, Kagi D, Mueller C. Differential contribution of Fas- and perforin-mediated mechanisms to the cell-mediated cytotoxic activity of naive and in vivo-primed intestinal intraepithelial lymphocytes. J. Immunol. 164(1), 398–403 (2000).
   PubMedGoogle Scholar
• Biedermann T, Kneilling M, Mailhammer R et al. Mast cells control neutrophil recruitment during T-cell-mediated delayed-type hypersensitivity reactions through tumor necrosis factor and macrophage inflammatory protein 2. J. Exp. Med. 192(10), 1441–1452 (2000).
   PubMed Web of Science ®Google Scholar
• Askenase PW, Szczepanik M, Itakura A, Kiener C, Campos RA. Extravascular T-cell recruitment requires initiation begun by Valpha14+ NKT cells and B-1 B-cells. Trends Immunol. 25(8), 441–449 (2004).
   PubMed Web of Science ®Google Scholar
• Tsuji RF, Kawikova I, Ramabhadran R et al. Early local generation of C5a initiates the elicitation of contact sensitivity by leading to early T-cell recruitment. J. Immunol. 165(3), 1588–1598 (2000).
   PubMed Web of Science ®Google Scholar
• Pastore S, Mascia F, Mariotti F, Dattilo C, Girolomoni G. Chemokine networks in inflammatory skin diseases. Eur. J. Dermatol. 14(4), 203–208 (2004).
   PubMed Web of Science ®Google Scholar
• Dilulio NA, Engeman T, Armstrong D, Tannenbaum C, Hamilton TA, Fairchild RL. Groalpha-mediated recruitment of neutrophils is required for elicitation of contact hypersensitivity. Eur. J. Immunol. 29(11), 3485–3495 (1999).
   PubMed Web of Science ®Google Scholar
• Engeman T, Gorbachev AV, Kish DD, Fairchild RL. The intensity of neutrophil infiltration controls the number of antigen-primed CD8 T-cells recruited into cutaneous antigen challenge sites. J. Leukoc. Biol. 76(5), 941–949 (2004).
   PubMed Web of Science ®Google Scholar
• Trautmann A, Akdis M, Kleemann D et al. T-cell-mediated Fas-induced keratinocyte apoptosis plays a key pathogenetic role in eczematous dermatitis. J. Clin. Invest. 106(1), 25–35 (2000).
   PubMed Web of Science ®Google Scholar
• Akdis M, Trautmann A, Klunker S et al. T-helper (Th) 2 predominance in atopic diseases is due to preferential apoptosis of circulating memory/effector Th1 cells. FASEB J. 17(9), 1026–1035 (2003).
   PubMed Web of Science ®Google Scholar
• Trautmann A, Akdis M, Schmid-Grendelmeier P et al. Targeting keratinocyte apoptosis in the treatment of atopic dermatitis and allergic contact dermatitis. J. Allergy Clin. Immunol. 108(5), 839–846 (2001).
   PubMed Web of Science ®Google Scholar
• Grabbe S, Schwarz T. Immunoregulatory mechanisms involved in elicitation of allergic contact hypersensitivity. Immunol. Today 19(1), 37–44 (1998).
   PubMedGoogle Scholar
• Dubois B, Chapat L, Goubier A, Kaiserlian D. CD4+CD25+ T-cells as key regulators of immune responses. Eur. J. Dermatol. 13(2), 111–116 (2003).
   PubMed Web of Science ®Google Scholar
• Desvignes C, Etchart N, Kehren J, Akiba I, Nicolas JF, Kaiserlian D. Oral administration of hapten inhibits in vivo induction of specific cytotoxic CD8+ T-cells mediating tissue inflammation: a role for regulatory CD4+ T-cells. J. Immunol. 164(5), 2515–2522 (2000).
   PubMed Web of Science ®Google Scholar
• Desvignes C, Bour H, Nicolas JF, Kaiserlian D. Lack of oral tolerance but oral priming for contact sensitivity to dinitrofluorobenzene in major histocompatibility complex class II-deficient mice and in CD4+ T-cell-depleted mice. Eur. J. Immunol. 26(8), 1756–1761 (1996).
   PubMedGoogle Scholar
• Ruckert R, Brandt K, Hofmann U, Bulfone-Paus S, Paus R. IL-2-IgG2b fusion protein suppresses murine contact hypersensitivity in vivo. J. Invest. Dermatol. 119(2), 370–376 (2002).
   PubMed Web of Science ®Google Scholar
• Gorbachev AV, Fairchild RL. CD4+ T-cells regulate CD8+ T-cell-mediated cutaneous immune responses by restricting effector T-cell development through a Fas ligand-dependent mechanism. J. Immunol. 172(4), 2286–2295 (2004).
   PubMed Web of Science ®Google Scholar
• Dearman RJ, Kimber I. Role of CD4(+) T-helper 2-type cells in cutaneous inflammatory responses induced by fluorescein isothiocyanate. Immunology 101, 442–451 (2000).
   PubMedGoogle Scholar
• Takeshita KYT, Akira S, Gantner F, Bacon KB. Essential role of MHC II-independent CD4+ T-cells, IL-4 and STAT6 in contact hypersensitivity induced by fluorescein isothiocyanate in the mouse. Int. Immunol. 16(5), 685–695 (2004).
   PubMed Web of Science ®Google Scholar
• Kondo S, Beissert S, Wang B. Hyporesponsiveness in contact hypersensitivity and irritant contact dermatitis in CD4 gene targeted mouse. J. Invest. Dermatol. 106, 993–1000 (1996).
   PubMedGoogle Scholar
• Wang B, Fujisawa H, Zhuang L et al. CD4+ Th1 and CD8+ Type 1 cytotoxic T-cells both play a crucial role in the full development of contact hypersensitivity. J. Immunol. 165(12), 6783–6790 (2000).
   PubMed Web of Science ®Google Scholar
• Bachmann MF, Oxenius A, Mak TW, Zinkernagel RM. T-cell development in CD8-/- mice. Thymic positive selection is biased toward the helper phenotype. J. Immunol. 155(8), 3727–3733 (1995).
   PubMedGoogle Scholar
• Hornquist CE, Ekman L, Grdic KD, Schon K, Lycke NY. Paradoxical IgA immunity in CD4-deficient mice. Lack of cholera toxin-specific protective immunity despite normal gut mucosal IgA differentiation. J. Immunol. 155(6), 2877–2887 (1995).
   PubMedGoogle Scholar
• Locksley RM, Reiner SL, Hatam F, Littman DR, Killeen N. Helper T-cells without CD4: control of leishmaniasis in CD4-deficient mice. Science 261(5127), 1448–1451 (1993).
   PubMed Web of Science ®Google Scholar
• Askenase PW. Yes T-cells, but three different T-cells (αβ, γδ and NK T-cells), and also B-1 cells mediate contact sensitivity. Clin. Exp. Immunol. 125(3), 345–350 (2001).
   PubMedGoogle Scholar
• Yokozeki H, Watanabe K, Igawa K, Miyazaki Y, Katayama I, Nishioka K. γδ T-cells assist αβ T-cells in the adoptive transfer of contact hypersensitivity to para-phenylenediamine. Clin. Exp. Immunol. 125(3), 351–359 (2001).
   PubMedGoogle Scholar
• Campos RA, Szczepanik M, Itakura A et al. Cutaneous immunization rapidly activates liver invariant Va14 NKT cells stimulating B-1 B-cells to initiate T-cell recruitment for elicitation of contact sensitivity. J. Exp. Med. 198(12), 1785–1796 (2003).
   PubMed Web of Science ®Google Scholar
• Sinigaglia F, Scheidegger D, Garotta G, Scheper R, Pletscher M, Lanzavecchia A. Isolation and characterization of Ni-specific T-cell clones from patients with Ni-contact dermatitis. J. Immunol. 135(6), 3929–3932 (1985).
   PubMedGoogle Scholar
• Cavani A, Mei D, Guerra E et al. 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. Invest. Dermatol. 111(4), 621–628 (1998).
   PubMed Web of Science ®Google Scholar
• Basketter D, Gerberick F, Kimber I, Willis C. Toxicology of Contact Dermatitis. Allergy, Irritancy and Urticaria. John Wiley & Sons, Chichester, UK (1999).
   Google Scholar
• Rycroft RJG, Menné T, Frosch PJ, Lepoittevin JP. Textbook of Contact Dermatitis. Second edition. Springer, Berlin, Germany (2001).
   Google Scholar
• Cavani A. Immune Mechanisms in Allergic Contact Dermatitis. L. Biosciences, TX, USA, 147 (2005).
   Google Scholar
• Bos JD. Skin Immune System – Cutaneous Immunology and Clinical Immunodermatology. CRC Press LLC, FL, USA (2005).
   Google Scholar
• Norris DA. Immune Mechanisms in Cutaneous Disease. Second edition. Marcel Dekker Inc., NY, USA (1989).
   Google Scholar