Contact hypersensitivity dermatitis occurs when the immune system mounts a response to chemicals the body comes into contact with via the skin. Alone these chemicals would be too small for the immune system to respond to, but they are all capable of binding to proteins within the body, a process termed haptenation. In most individuals this is harmless however in some individuals an immune response against chemicals bound to self proteins is mounted leading to inflammation of the skin at the contact site. Many commonly encountered chemicals are capable of acting as contact sensitizers, these include petrochemicals, heavy metal ions (i.e Nickel) and some plant extracts (i.e urushiol from poison ivy).
DNCB-induced Contact Dermatitis
The 2,4-Dinitrochlorobenzene (DNCB) induced contact dermatitis model is Th1 mediated with IFN-g production by both CD4+ and CD8+ cells observed and increased IL-12p40 mRNA observed in the draining lymph node. Cell mediated responses are thought to be of particular importance in the pathology associated with challenge of sensitised individuals.
FITC-induced Contact Dermatitis
The Fluorescein isothyocyanate (FITC) induced contact dermatitis model is mediated by the Th2 pathway. Unlike many contact hypersensitivity reactions which induce strongly cytotoxic T cell mediated responses; the response to FITC challenge exhibits many of the hallmarks of atopic dermatitis; Local eosinophilia, mast cells infiltration, Anti-FITC IgE and IL-4 and IL-10 production by CD4+ cells are observed following sensitisation. In addition immediate and late phase responses are observed. Work to dissect the pathological mechanism has taken place, yielding the following results; The passive transfer of immune sera results in a rapid transient response to FITC challenge (peaking 15-30 minutes, returning to normal by 24hrs), The adoptive transfer of LN cells from sensitised mice results in a more delayed and sustained ear swelling, The depletion of CD4+ cells prior to adoptive transfer prevents ear swelling following application of FITC. These results suggest that IgE is responsible for the immediate phase of the response to FITC application while CD4+ cells sustain the response.
It is becoming apparent that a role for the Th17 pathway may also be important in the development of contact hypersensitivity and allergic responses, and has been implicated in the FITC induced contact dermatitis model. The Aryl hydrocarbon receptor (AhR) activation is a cofactor in the development of Th17 responses and AhR null mice have been shown have impaired Langerhans cell maturation and as a result impaired responses to FITC sensitisation.