Analysis of the mononuclear inflammatory cell infiltrate in the non-tumorigenic, pre-tumorigenic and tumorigenic keratinocytic hyperproliferative lesions of the skin.
BACKGROUND
The keratinocytic hyperproliferative lesions include non-tumorigenic, pre-tumorigenic (actinic keratoses, AK), and tumorigenic (squamous cell carcinomas, SCC) conditions. Although mononuclear inflammatory cell infiltrate (MICs) is a constant feature in these lesions, their immunophenotypic characterization is still incomplete. We hypothesized that the development of non-tumorigenic, pre-tumorigenic, and tumorigenic keratinocytic hyperproliferative lesions is associated with alterations in the mononuclear inflammatory cell infiltrate in response to altered antigenicity of the lesional cells. This study tries to test this hypothesis and to characterize MICs in these lesions.


METHODS
Fifty lesions (non-tumorigenic lesions, 29; AK, 9 and SCC, 12) were examined using immunoperoxidase staining methods and antibodies targeting histiocytes (CD68), T cells (CD3), B cells (CD20), and T cells with cytotoxic potential (TIA-1).


RESULTS
As compared to the normal skin, the development of the keratinocytic hyperproliferative lesions (normal skin; non-tumorigenic; AK and SCC) was associated with a statistically significant increase (p = <0.05) in: (1) CD20+ B lymphocytes (0.0 +/- 0.0 vs. 3.1 +/- 0.5 vs. 7.5 +/- 0.3 vs. 14.5 +/- 5.5); (2) CD68 histiocytes (4.0 +/- 1.0 vs. 26.5 +/- 3.9 vs. 23 +/- 1.9 vs. 41.3 +/- 6.8); (3) CD3+ T lymphocytes (3.0 +/- 1.1 vs. 58.3 +/- 10.3 vs. 54.5 +/- 0.2 vs. 41.0 +/- 16.0); and (4) TIA-1+ cytotoxic T cells (1.8 +/- 0.4 vs. 2.9 +/- 0.7 vs. 9.6 +/- 1.1 vs. 13.7 +/- 5.2).


CONCLUSIONS
The increase in the number of infiltrating mononuclear cells in all pathologic lesions compared to normal skin may reflect increased antigenicity of the lesional cells. Both humoral and cell mediated immunity are involved in these lesions.
Hussein
Mahmoud R
MR
Department of Pathology, Assiut University Hospitals, Faculty of Medicine, Assiut University, Egypt. mrh17@swissinfo.org
Ahmed
Rabab A
RA
D015703:Antigens, CD / Q000032:analysis; D016175:B-Lymphocyte Subsets / Q000276:immunology; D002471:Cell Transformation, Neoplastic / Q000276:immunology* / Q000473:pathology; D002478:Cells, Cultured; D006801:Humans; D007642:Keratosis / Q000276:immunology / Q000473:pathology; D016246:Lymphocytes, Tumor-Infiltrating / Q000276:immunology; D039102:Poly(A)-Binding Proteins / Q000032:analysis; D012867:Skin / Q000166:cytology / Q000276:immunology / Q000473:pathology; D012878:Skin Neoplasms / Q000276:immunology* / Q000473:pathology; D000074019:T-Cell Intracellular Antigen-1; D016176:T-Lymphocyte Subsets / Q000276:immunology; D014407:Tumor Cells, Cultured
D015703:Antigens, CD; D039102:Poly(A)-Binding Proteins; D000074019:T-Cell Intracellular Antigen-1; C071558:TIA1 protein, human