Allergic contact dermatitis: the cellular effectors

Kimber, Ian; Dearman, Rebecca J.

doi:10.1034/j.1600-0536.2002.460101.x

Cited by 130 publications

(88 citation statements)

References 41 publications

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“…HLArestricted Ni-reactive T cell lines and clones of both CD4 and CD8 phenotypes have repeatedly been isolated by NiSO 4 or NiCl 2 stimulation of T cells from peripheral blood or skin lesions of allergic patients and even from nonsensitized individuals (1,9,44,45). Recent data imply that Ni 2ϩ mediate TCR/MHC contact by formation of complexes involving amino acids of TCR and/or MHC as coordination partners (24,46,47).…”

Section: Discussionmentioning

confidence: 99%

Metal-Protein Complex-Mediated Transport and Delivery of Ni2+ to TCR/MHC Contact Sites in Nickel-Specific Human T Cell Activation

Thierse

Moulon

Allespach

et al. 2004

The Journal of Immunology

100

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Nickel allergy clearly involves the activation of HLA-restricted, skin-homing, Ni-specific T cells by professional APCs. Nevertheless, knowledge concerning the molecular details of metal-protein interactions underlying the transport and delivery of metal ions to APC during the early sensitization phase and their interactions with HLA and TCRs is still fragmentary. This study investigates the role of human serum albumin (HSA), a known shuttling molecule for Ni2+ and an often-disregarded, major component of skin, in these processes. We show that Ni-saturated HSA complexes (HSA-Ni) induce and activate Ni-specific human T cells as potently as Ni salt solutions when present at equimolar concentrations classically used for in vitro T cell stimulation. However, neither HSA itself nor its Ni-binding N-terminal peptide are involved in determining the specificity of antigenic determinants. In fact, HSA could be replaced by xenogeneic albumins exhibiting sufficient affinity for Ni2+ as determined by surface plasmon resonance (Biacore technology) or atomic absorption spectroscopy. Moreover, despite rapid internalization of HSA-Ni by APC, it was not processed into HLA-associated epitopes recognizable by Ni-specific T cells. In contrast, the presence of HSA-Ni in the vicinity of transient contacts between TCR and APC-exposed HLA molecules appeared to facilitate a specific transfer of Ni2+ from HSA to high-affinity coordination sites created at the TCR/HLA-interface.

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Section: Discussionmentioning

confidence: 99%

Metal-Protein Complex-Mediated Transport and Delivery of Ni2+ to TCR/MHC Contact Sites in Nickel-Specific Human T Cell Activation

Thierse

Moulon

Allespach

et al. 2004

The Journal of Immunology

100

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“…Some investigations in mice found CHS to be associated with CD4 ϩ T lymphocyte function and to be compromised when such cells were deleted (15,16). However, there is growing evidence that in many instances the predominant effector cell in CHS may be a CD8 ϩ T lymphocyte (13,17,18). Wang et al (17) clearly demonstrated that the deletion of CD8 ϩ Tc1 cells had a more significant suppressive effect than the deletion of CD4 ϩ Th1 cells in CHS responses to 2,4-dinitrofluorobenzene (DNFB).…”

Section: T-bet Is Known As a Th1 Lineage Commitment Transcription Facmentioning

confidence: 99%

“…Contact dermatitis and CHS are delayed-type hypersensitivity reactions that are mediated by haptenspecific T cells (12). Skin sensitization resulting in contact dermatitis and CHS is dependent on the initiation of specific T lymphocyte responses (11,13). Until recently it was believed that the most important cells in these responses were CD4 ϩ T lymphocytes.…”

Section: T-bet Is Known As a Th1 Lineage Commitment Transcription Facmentioning

confidence: 99%

Th1 and Type 1 Cytotoxic T Cells Dominate Responses in T-bet Overexpression Transgenic Mice That Develop Contact Dermatitis

Ishizaki¹,

Yamada²,

Yoh

et al. 2007

The Journal of Immunology

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Contact dermatitis in humans and contact hypersensitivity (CHS) in animal models are delayed-type hypersensitivity reactions mediated by hapten-specific T cells. Recently, it has become clear that both CD4+ Th1 and CD8+ type 1 cytotoxic T (Tc1) cells can act as effectors in CHS reactions. T-bet has been demonstrated to play an important role in Th1 and Tc1 cell differentiation, but little is known about its contribution to CHS. In the present study, we used C57BL/6 mice transgenic (Tg) for T-bet to address this issue. These Tg mice, which overexpressed T-bet in their T lymphocytes, developed dermatitis characterized by swollen, flaky, and scaly skin in regions without body hair. Skin histology showed epidermal hyperkeratosis, neutrophil, and lymphocyte infiltration similar to that seen in contact dermatitis. T-bet overexpression in Tg mice led to elevated Th1 Ig (IgG2a) and decreased Th2 Ig (IgG1) production. Intracellular cytokine analyses demonstrated that IFN-γ was increased in both Th1 and Tc1 cells. Furthermore, Tg mice had hypersensitive responses to 2,4-dinitrofluorobenzene, which is used for CHS induction. These results suggest that the level of expression of T-bet might play an important role in the development of contact dermatitis and that these Tg mice should be a useful model for contact dermatitis.

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“…21 The primary effector cell in DHT is CD4 TL while the main effector cell in ACD is CD8 TL, which has its action supported by type 1 auxiliary TL and suppressed by other CD4 T cells. 47,88 A series of findings, described below, led to these conclusions.…”

Section: Lymphocytes Effector Lymphocytesmentioning

confidence: 97%

Imunopatologia da dermatite de contato alérgica

Martins

Reis

2011

An. Bras. Dermatol.

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Allergic contact dermatitis is the consequence of an immune reaction mediated by T cells against low molecular weight chemicals known as haptens. It is a common condition that occurs in all races and age groups and affects the quality of life of those who present it. The immunological mechanism of this disease has been reviewed in recent decades with significant advance in its understanding. The metabolism and pathway of the haptens as well as the activation and mechanism of action of the cells responsible for both the immune reaction and its completion are discussed in this article. Keywords: Allergy and immunology; Dermatitis, allergic contact; Dermatitis, contact; Hypersensitivity Resumo: A dermatite de contato alérgica é consequência de uma reação imune mediada por células T contra químicos de baixo peso molecular, denominados haptenos. É uma condição frequente que ocorre em todas as raças e faixas etárias e afeta a qualidade de vida de seus portadores. O mecanismo imunológico desta doença vem sendo revisto nas últimas décadas com significativo avanço no seu entendimento. A metabolização e o caminho dos haptenos, bem como a formação e o mecanismo de ação das células responsáveis tanto pela reação quanto pelo seu término, são discutidos neste artigo. Palavras-chave: Alergia e imunologia; Hipersensibilidade; Dermatite de contato; Dermatites alérgicas de contato

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Allergic contact dermatitis: the cellular effectors

Cited by 130 publications

References 41 publications

Metal-Protein Complex-Mediated Transport and Delivery of Ni2+ to TCR/MHC Contact Sites in Nickel-Specific Human T Cell Activation

Metal-Protein Complex-Mediated Transport and Delivery of Ni2+ to TCR/MHC Contact Sites in Nickel-Specific Human T Cell Activation

Th1 and Type 1 Cytotoxic T Cells Dominate Responses in T-bet Overexpression Transgenic Mice That Develop Contact Dermatitis

Imunopatologia da dermatite de contato alérgica

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