Abstract
Objective. Localized scleroderma causes thickening of the skin due to excessive collagen deposition. This condition has clinical and histopathological similarities to chronic graft- vs -host disease. We wanted to identify whether chimeric cells are present in the affected tissue in localized scleroderma and to further investigate the role of chimerism by immunophenotyping the chimeric cells. We hypothesize that the presence of chimerism and immunotypic chimeric cells will lend to an understanding of the pathogenesis of localized scleroderma and possible mechanisms by which chimeric cells participate in autoimmunity. Methods. We studied skin biopsies from 18 localized scleroderma patients and compared them with concurrent biopsies from unaffected skin in a subset of patients. Skin biopsies from morphoea and linear scleroderma patients were analysed for the presence of chimeric cells using male-female (X, Y) differences. Cell surface markers (CD4, CD8, CD19/20, CD68, S100, CD14 and CD56) were determined for cell phenotyping of chimeric cells. Results. Overall, the affected tissue contained a greater number of lymphocytic inflammatory cells. In the affected tissue, 38% of the total chimeric cells were CD68+ (dendritic cell, monocyte and macrophage marker), 29% Langerin/S100+ (dendritic cell marker), 26% CD8+ (cytotoxic T-lymphocyte marker), 20% CD19/20+ (B-lymphocyte marker), 14% CD4+ (T-helper lymphocyte) and 0% CD56+ (natural killer cell marker). Conclusions. We report that not only are chimeric cells present in affected localized scleroderma lesions but they also are more likely to be dendritic cells and B lymphocytes suggesting a role in the pathogenesis of localized scleroderma.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 398-402 |
| Number of pages | 5 |
| Journal | Rheumatology |
| Volume | 46 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 2007 |
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Keywords
- cGVHD
- Chimerism
- Localized scleroderma
- Morphoea
ASJC Scopus subject areas
- Neuroscience(all)
- Rheumatology
Cite this
Immunophenotyping of chimeric cells in localized scleroderma. / McNallan, K. T.; Aponte, C.; el-Azhary, R.; Mason, Thomas; Nelson, A. M.; Paat, J. J.; Crowson, Cynthia; Reed, Ann M.
In: Rheumatology, Vol. 46, No. 3, 03.2007, p. 398-402.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Immunophenotyping of chimeric cells in localized scleroderma
AU - McNallan, K. T.
AU - Aponte, C.
AU - el-Azhary, R.
AU - Mason, Thomas
AU - Nelson, A. M.
AU - Paat, J. J.
AU - Crowson, Cynthia
AU - Reed, Ann M.
PY - 2007/3
Y1 - 2007/3
N2 - Objective. Localized scleroderma causes thickening of the skin due to excessive collagen deposition. This condition has clinical and histopathological similarities to chronic graft- vs -host disease. We wanted to identify whether chimeric cells are present in the affected tissue in localized scleroderma and to further investigate the role of chimerism by immunophenotyping the chimeric cells. We hypothesize that the presence of chimerism and immunotypic chimeric cells will lend to an understanding of the pathogenesis of localized scleroderma and possible mechanisms by which chimeric cells participate in autoimmunity. Methods. We studied skin biopsies from 18 localized scleroderma patients and compared them with concurrent biopsies from unaffected skin in a subset of patients. Skin biopsies from morphoea and linear scleroderma patients were analysed for the presence of chimeric cells using male-female (X, Y) differences. Cell surface markers (CD4, CD8, CD19/20, CD68, S100, CD14 and CD56) were determined for cell phenotyping of chimeric cells. Results. Overall, the affected tissue contained a greater number of lymphocytic inflammatory cells. In the affected tissue, 38% of the total chimeric cells were CD68+ (dendritic cell, monocyte and macrophage marker), 29% Langerin/S100+ (dendritic cell marker), 26% CD8+ (cytotoxic T-lymphocyte marker), 20% CD19/20+ (B-lymphocyte marker), 14% CD4+ (T-helper lymphocyte) and 0% CD56+ (natural killer cell marker). Conclusions. We report that not only are chimeric cells present in affected localized scleroderma lesions but they also are more likely to be dendritic cells and B lymphocytes suggesting a role in the pathogenesis of localized scleroderma.
AB - Objective. Localized scleroderma causes thickening of the skin due to excessive collagen deposition. This condition has clinical and histopathological similarities to chronic graft- vs -host disease. We wanted to identify whether chimeric cells are present in the affected tissue in localized scleroderma and to further investigate the role of chimerism by immunophenotyping the chimeric cells. We hypothesize that the presence of chimerism and immunotypic chimeric cells will lend to an understanding of the pathogenesis of localized scleroderma and possible mechanisms by which chimeric cells participate in autoimmunity. Methods. We studied skin biopsies from 18 localized scleroderma patients and compared them with concurrent biopsies from unaffected skin in a subset of patients. Skin biopsies from morphoea and linear scleroderma patients were analysed for the presence of chimeric cells using male-female (X, Y) differences. Cell surface markers (CD4, CD8, CD19/20, CD68, S100, CD14 and CD56) were determined for cell phenotyping of chimeric cells. Results. Overall, the affected tissue contained a greater number of lymphocytic inflammatory cells. In the affected tissue, 38% of the total chimeric cells were CD68+ (dendritic cell, monocyte and macrophage marker), 29% Langerin/S100+ (dendritic cell marker), 26% CD8+ (cytotoxic T-lymphocyte marker), 20% CD19/20+ (B-lymphocyte marker), 14% CD4+ (T-helper lymphocyte) and 0% CD56+ (natural killer cell marker). Conclusions. We report that not only are chimeric cells present in affected localized scleroderma lesions but they also are more likely to be dendritic cells and B lymphocytes suggesting a role in the pathogenesis of localized scleroderma.
KW - cGVHD
KW - Chimerism
KW - Localized scleroderma
KW - Morphoea
UR - http://www.scopus.com/inward/record.url?scp=33847413649&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33847413649&partnerID=8YFLogxK
U2 - 10.1093/rheumatology/kel297
DO - 10.1093/rheumatology/kel297
M3 - Article
C2 - 17085771
AN - SCOPUS:33847413649
VL - 46
SP - 398
EP - 402
JO - Rheumatology (United Kingdom)
JF - Rheumatology (United Kingdom)
SN - 1462-0324
IS - 3
ER -