Immunological mechanisms of contact hypersensitivity in mice

TY - JOUR

T1 - Immunological mechanisms of contact hypersensitivity in mice

AU - Christensen, Anne Deen

AU - Haase, Claus

PY - 2012/1

Y1 - 2012/1

N2 - Contact hypersensitivity (CHS) is an animal model in which the immunological mechanisms of allergic contact dermatitis (ACD) in humans can be studied but is also widely used in the study of many basic immunological mechanisms. In CHS, a pre-sensitized animal is re-exposed to an antigen, thereby eliciting an immunological reaction at the site of antigen exposure. CHS consists of two phases: sensitization and elicitation phase. In the sensitization phase, the first contact of the skin with a hapten leads to binding of the hapten to an endogenous protein in the skin where they form hapten-carrier complexes which are immunogenic. The hapten-carrier complex is taken up by Langerhans cells (LCs) and dermal dendritic cells (dDCs) which migrate from the epidermis to the draining lymph node. Here, they present the haptenated peptides to naive T cells which are subsequently activated. The newly activated T cells proliferate and migrate out of the lymph node and into circulation. In the elicitation phase, re-exposure of the skin to the hapten activates the specific T cells in the dermis and triggers the inflammatory process responsible for the cutaneous lesions. Originally CHS was regarded as being solely driven by T cells but recently other cell types such as B1 cells, natural killer (NK) T cells and NK cells have shown to mediate important functions during the response as well. Here, we have described the molecular and cellular pathways in the development of CHS and have focused on recent advances and novel knowledge in the understanding of the immunoregulatory mechanisms involved in CHS.

AB - Contact hypersensitivity (CHS) is an animal model in which the immunological mechanisms of allergic contact dermatitis (ACD) in humans can be studied but is also widely used in the study of many basic immunological mechanisms. In CHS, a pre-sensitized animal is re-exposed to an antigen, thereby eliciting an immunological reaction at the site of antigen exposure. CHS consists of two phases: sensitization and elicitation phase. In the sensitization phase, the first contact of the skin with a hapten leads to binding of the hapten to an endogenous protein in the skin where they form hapten-carrier complexes which are immunogenic. The hapten-carrier complex is taken up by Langerhans cells (LCs) and dermal dendritic cells (dDCs) which migrate from the epidermis to the draining lymph node. Here, they present the haptenated peptides to naive T cells which are subsequently activated. The newly activated T cells proliferate and migrate out of the lymph node and into circulation. In the elicitation phase, re-exposure of the skin to the hapten activates the specific T cells in the dermis and triggers the inflammatory process responsible for the cutaneous lesions. Originally CHS was regarded as being solely driven by T cells but recently other cell types such as B1 cells, natural killer (NK) T cells and NK cells have shown to mediate important functions during the response as well. Here, we have described the molecular and cellular pathways in the development of CHS and have focused on recent advances and novel knowledge in the understanding of the immunoregulatory mechanisms involved in CHS.

U2 - 10.1111/j.1600-0463.2011.02832.x

DO - 10.1111/j.1600-0463.2011.02832.x

M3 - Review

C2 - 22151305

SN - 0903-465X

VL - 120

SP - 1

EP - 27

JO - APMIS. Supplementum

JF - APMIS. Supplementum

IS - 1

ER -