2006
DOI: 10.3892/or.15.2.347
|View full text |Cite
|
Sign up to set email alerts
|

Expression of the CD1a molecule in B- and T-lymphoproliferative skin conditions

Abstract: The skin immune system is characterized by the presence of two types of CD1a expressing cells: Langerhans cells and dermal dendritic cells, which are professional antigen processing and presenting cells. It is well established that several dermatoses are associated with T-cell mediated immune responses. In these pathological skin conditions, T-cells are activated by professional antigen presenting cells and dendritic cells are the most potent antigen presenting cells for both Thelper cells and T-cytotoxic cell… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
31
0
5

Year Published

2008
2008
2019
2019

Publication Types

Select...
7
1

Relationship

0
8

Authors

Journals

citations
Cited by 24 publications
(36 citation statements)
references
References 25 publications
0
31
0
5
Order By: Relevance
“…This increase is also seen in other T-cell proliferations, like lymphomatoid papulosis, but not in B-cell lymphomas. [15] Goteri et al . showed that an increased dermal (but not epidermal) CD1a+ cells correlated with the density of the neoplastic infiltrate.…”
Section: Discussionmentioning
confidence: 99%
“…This increase is also seen in other T-cell proliferations, like lymphomatoid papulosis, but not in B-cell lymphomas. [15] Goteri et al . showed that an increased dermal (but not epidermal) CD1a+ cells correlated with the density of the neoplastic infiltrate.…”
Section: Discussionmentioning
confidence: 99%
“…This fact also helps to rule out that H&N-KD (or any antigenic stimulation in the lesions) originates from Langerhans cells. It is possible that the B-cell proliferation hampers the recruitment of CD1a+ cells in T-cell-rich areas via certain inhibitory cytokines (Pigozzi et al, 2006).…”
Section: Discussionmentioning
confidence: 99%
“…Dentro de las teorías propuestas se encuentran una predisposición genética (por la relación con determinados alelos de HLA clase II en población judía), 5 una estimulación antigénica crónica que llevaría a una proliferación clonal descontrolada de linfocitos T (dado el aumento en el número de células dendríticas y la mayor expresión de B7/CD28 y CD40/CD40L en lesiones tempranas, [7][8][9] así como la mayor expresión de receptores tipo Toll 2, 4 y 9 en queratinocitos), 10 infecciones (particularmente por estafilococo aureus, ya que se ha demostrado su colonización en MF eritrodérmica y en síndrome de Sézary; 11 a diferencia de algunos linfomas cutáneos agresivos, no se ha logrado demostrar una asociación entre MF y virus de Epstein Barr o HTLV-1 12,13 e inmunosupresión (por la asociación infrecuente con trasplantados de órganos sólidos 14 y pacientes portadores de VIH).…”
Section: Etiopatogeniaunclassified