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Intercellular adhesion molecule-I (ICAM-I) expression correlated to inflammation
S Lisby1, E Ralfkiaer, R Rothlein
1Department of Dermatology, Bispebjerg Hospital, Copenhagen, Denmark.
The British Journal of Dermatology
|April 1, 1989
Summary
Intercellular adhesion molecule-I (ICAM-I) expression on skin cells decreased with successful psoriasis treatment. Increased ICAM-I correlated with disease severity and relapse in patients undergoing PUVA therapy.
Area of Science:
- Dermatology
- Immunology
- Cell Biology
Background:
- Psoriasis is a chronic inflammatory skin condition.
- Intercellular adhesion molecule-I (ICAM-I) plays a role in immune cell adhesion and inflammation.
- The expression of ICAM-I in psoriatic lesions and its modulation by treatment are not fully understood.
Purpose of the Study:
- To investigate the presence and significance of ICAM-I on keratinocytes in psoriatic skin lesions.
- To evaluate the changes in ICAM-I expression during 8-methoxapsoralen and UVA (PUVA) treatment.
- To correlate ICAM-I expression with disease severity and immune cell infiltration.
Main Methods:
- Biopsies were taken from psoriatic skin lesions of five patients before and during PUVA treatment.
- Immunohistochemistry was used to assess ICAM-I expression on keratinocytes.
- Changes in mononuclear cell infiltrate and disease severity were also evaluated.
Main Results:
- ICAM-I was expressed on keratinocytes in psoriatic lesions.
- Responders to PUVA treatment showed reduced ICAM-I expression, decreased mononuclear cell infiltrate, and lessened disease severity.
- Patients who relapsed exhibited increased ICAM-I expression, more mononuclear cells, and worsening disease.
- HLA-DR expression on keratinocytes was variable and did not strongly correlate with disease severity.
Conclusions:
- ICAM-I expression on keratinocytes is a potential biomarker for monitoring psoriasis activity and response to PUVA treatment.
- Modulation of ICAM-I may be involved in the therapeutic effects of PUVA therapy in psoriasis.
- Further research is warranted to explore the therapeutic potential of targeting ICAM-I in psoriasis management.