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Vulvar lichen sclerosus: an immunologic study
F Scrimin1, S Rustja, O Radillo
1Department of Obstetrics and Gynaecology, University of Trieste, Italy.
Insights
Vulvar lichen sclerosus shows reduced T-cell counts and autoantibodies, but lacks evidence of local autoantibody production or a T-cell mediated response. This suggests non-autoimmune origins and supports symptomatic treatment like petroleum jelly.
Area of Science:
- Immunology
- Dermatology
- Pathogenesis of Vulvar Lichen Sclerosus
Background:
- Vulvar lichen sclerosus (VLS) is a chronic inflammatory skin condition with uncertain etiology.
- Understanding the immunologic profile of VLS is crucial for determining its pathogenesis and guiding treatment strategies.
Purpose of the Study:
- To investigate the seroimmunologic and immunohistochemical characteristics of VLS.
- To elucidate the potential role of immune cells and autoantibodies in the pathogenesis of VLS.
Main Methods:
- Comparative analysis of serum and tissue samples from VLS patients and healthy controls.
- Assessment of T lymphocytes (CD3, CD4, CD8), B lymphocytes (CD19, CD21), natural killer cells (CD56), macrophages, immunoglobulins (IgG, IgM), and complement fractions (C3c, C4).
- Utilized immunohistochemistry and a scoring system for quantitative cell analysis in tissue.
Main Results:
- VLS patients exhibited significantly lower circulating CD3 and CD4 lymphocytes and higher autoantibody levels compared to controls.
- Tissue analysis revealed reduced epidermal and dermal CD2, CD3, CD4, and CD8 cells in VLS patients.
- Absence of natural killer cells (CD56) and B lymphocytes (CD19-CD21) in affected VLS tissues, with no increased IgG, IgM, or C3 deposits.
Conclusions:
- The findings do not support a T cell-mediated or autoimmune pathogenesis for VLS.
- The absence of local B cell markers (CD19, CD21) excludes local autoantibody production.
- The results help explain the limited efficacy of systemic corticosteroids and support the use of emollients for symptom relief in VLS.
Objective:
To investigate the seroimmunologic (CD3, CD4, CD8 lymphocytes, C3c and C4 complement fractions, and several autoantibodies) and immunohistochemical (T lymphocyte subpopulations, B lymphocytes, natural killer cells, macrophages, immunoglobulin [Ig] G, Ig M, and C3c complement fraction) characteristics of vulvar lichen sclerosus.
Methods:
Serum samples from 68 women with histologically proven lichen sclerosus were compared with those from 53 healthy controls, and tissue samples from 14 of 68 women chosen at random were compared with those from 14 of 53 healthy controls. A scoring system was constructed to compare the number of cells in the tissue.
Results:
Patients had significantly lower counts of circulating lymphocytes CD3 and CD4 than controls (P < .05) and a higher number of autoantibodies (P < .01). Analysis of the tissue samples confirmed a lower number of CD2 cells (two-tailed P = .002 in epidermis, .005 in dermis), CD3 cells (two-tailed P = .001 in epidermis and in dermis), CD4 cells (two-tailed P = .002 in epidermis, .011 in dermis), and CD8 cells (two-tailed P = .002 in epidermis, .051 in dermis) in subjects than in controls. Numbers of monocyte-macrophage cells were similar in the epidermis but different in the dermis (two-tailed P = .003). No natural killer CD56 cells or B lymphocytes (CD19-CD21) were detected in the affected areas. Deposits of IgG, IgM, and C3 were no greater in biopsy specimens of patients than in those of controls.
Conclusion:
Vulvar lichen sclerosus is not caused by a T cell-mediated response, and a viral origin is unlikely. The absence of CD19 and CD21 cells excludes local production of autoantibodies. Our data do not confirm an autoimmune pathogenesis for vulvar lichen sclerosus but help explain why systemic cortisone is of no benefit and justify the use of petroleum jelly to relieve pruritus.